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Project Title:  Sclerostin's Role in Regulating Bone Formation during Long-term Simulated Microgravity and Subsequent Recovery Reduce
Fiscal Year: FY 2018 
Division: Human Research 
Research Discipline/Element:
HRP HHC:Human Health Countermeasures
Start Date: 10/06/2014  
End Date: 11/06/2017  
Task Last Updated: 03/23/2018 
Download report in PDF pdf
Principal Investigator/Affiliation:   Bloomfield, Susan A. Ph.D. / Texas A&M University 
Address:  Department of Health & Kinesiology 
400 Harvey Mitchell Pkwy, Suite 300 
College Station , TX 77843-4375 
Email: sbloom@tamu.edu 
Phone: 979-845-2871  
Congressional District: 17 
Web:  
Organization Type: UNIVERSITY 
Organization Name: Texas A&M University 
Joint Agency:  
Comments:  
Project Information: Grant/Contract No. NNX15AB05G 
Responsible Center: NASA JSC 
Grant Monitor: Norsk, Peter  
Center Contact:  
Peter.norsk@nasa.gov 
Solicitation / Funding Source: 2013 HERO NNJ13ZSA002N-Crew Health (FLAGSHIP & NSBRI) 
Grant/Contract No.: NNX15AB05G 
Project Type: GROUND 
Flight Program:  
TechPort: No 
No. of Post Docs:
No. of PhD Candidates:
No. of Master's Candidates:
No. of Bachelor's Candidates:
No. of PhD Degrees:
No. of Master's Degrees:
No. of Bachelor's Degrees:
Human Research Program Elements: (1) HHC:Human Health Countermeasures
Human Research Program Risks: (1) Osteo:Risk Of Early Onset Osteoporosis Due To Spaceflight (No longer used, July 2020)
Human Research Program Gaps: (1) Osteo04:We do not know the contribution of each risk factor on bone loss and recovery of bone strength, and which factors are the best targets for countermeasure application (IRP Rev E)
Flight Assignment/Project Notes: NOTE: Extended to 11/06/2017 per NSSC information (Ed., 12/7/17)

NOTE: Extended to 8/31/2017 per NSSC information (Ed., 1/24/17)

NOTE: Extended to 10/05/2016 per NSSC information (Ed., 10/28/15)

Task Description: The tissue sharing opportunity outlined in Appendix A, Item B (“Cerebral Spinal Fluid Production/Absorption....”) offers an exciting chance to study the evolution of changes over 90 days of hindlimb suspension (HLS) in a rodent model. Few laboratories have the capability or expertise to carry out HLS for such a long period; the impact of this experiment will be multiplied many-fold with piggyback projects making strategic use of other tissues harvested from these animals. This proposal focuses on tracking the evolution of changes in a protein important to bone integrity called sclerostin over the course of 90 days of unloading and then during the 90-day recovery phase. Importantly, we will also track alterations in the key physiological function sclerostin regulates in bone: osteoblast activity resulting in the formation of new bone.

Sclerostin is produced by osteocytes, the bone cells embedded in bone matrix and the key sensors of loading/unloading; it works to inhibit the Wnt-Beta catenin signaling pathway in osteoblasts, which normally stimulates bone formation activity. Most studies to date document an increase in osteocyte’s sclerostin expression with unloading, which provides the mechanism for the suppressed bone formation seen with HLS on Earth and, presumably, with microgravity exposure. A recent study examining the impact of a novel therapeutic agent (sclerostin antibody) on mice flown on STS-135 yielded very positive findings, suggesting that manipulating sclerostin expression could be an important therapeutic tool to augment the usual exercise countermeasures employed by astronauts. Hence it becomes critical, before any such systemic therapy is considered, to understand clearly the relationship between sclerostin expression and the functionally important outcome (bone formation activity) in multiple bone sites.

Because there is evidence that Sost, the gene encoding the protein sclerostin, is expressed differently in mid-shaft vs metaphyseal bone, we will assess sclerostin expression and histomorphometric measures of bone formation in 3 different bone compartments for each bone: mid-shaft cortical bone, cancellous bone of the metaphysis and the metaphyseal cortical shell. We propose to first study these outcomes in paired tibiae or femurs (unloaded bone) and in normally loaded humeri. With the availability of female mice in the parent study’s 2nd specific aim, we can then assess if there are gender differences in this response. Recently published data on spaceflown mice document an increase in bone volume in calvarial bone, raising the intriguing possibility that fluid shifts during spaceflight may increase fluid pressures in the rodent brain compartment, providing a mechanical loading of sorts to the skull. Hence, a third specific aim of our proposal, pending verification that calvarial bone can be made available, will assess sclerostin expression and bone formation variables in this unique site to test this hypothesis. At the end of one year’s intensive effort, then, we will have gained a much more clear picture of how this important regulatory molecule is altered by unloading and whether sclerostin antibody does present a viable therapeutic tool for maintaining bone integrity on long-duration missions. In addition, we will gain important fundamental knowledge about the time course of sclerostin expression and its relationship to bone formation rate with alterations in mechanical loading.

Research Impact/Earth Benefits: Phase III clinical trials testing the efficacy of sclerostin antibody (Scl-AB) are in progress, focusing on the value of this agent in reversing aging-related bone loss and osteoporosis. It will be very useful to have data on a physiologically relevant mammalian model (skeletally mature rats) yielding information on the efficacy of Scl-AB for bone loss due to prolonged disuse. This applies to individuals subjected to prolonged bed rest (complicated orthopedic injuries, frail elderly with severe illness) or to conditions like spinal cord injury or even stroke (if significant muscle paralysis is involved). Additionally, this study will provide a sex comparison, so we will have preliminary clues as to whether women might respond similarly as do men to this potent anabolic treatment.

Task Progress & Bibliography Information FY2018 
Task Progress: The parent protocol at University of California (UC)-Davis apparently experienced many delays. Shipments have been received as recently as August 2017. This Principal Investigator (PI) requested and received two no-cost extensions in order to complete these analyses, given the delays in tissue availability. This allowed for analyses to extend beyond the young male samples to include young female and older male samples. There must have been a decision at UC-Davis to modify time points at which rats were sacrificed (or allocation of time points for tissue-sharing opportunities), since we never received samples from 4-d hindlimb unloading (HU) nor 4-d Recovery groups. We did receive samples from 14-d HU and 14-d Recovery animals. Further, there were many time points for which we had only 2-4 specimens, so decided to strategically focus our analyses on those time points for which we received at least 6 samples in matching groups. This was an unexpected, but welcome outcome; originally, we were cautioned to not expect more than 3 samples/timepoint/group.

The only timepoint for which we received adequate numbers of samples from the female cohorts was at 14 d HU; hence, we were able to complete statistical analyses of sex differences for that one time point. These were the planned analyses; some are still in progress :

A. Peripheral quantitative computed tomography (for BMD, bone geometry)

a. Young males at 7, 14, 28, and 90 d of HU and 14, 28, and 90 d of recovery from HU

b. Old males at 14 and 90 d HU and 14 and 90 d of recovery from HU

c. Young females at 14 d HU

B. Static histomorphometry for % osteoid (new bone; index of formation activity) and for % osteoclast (bone resorbing) surfaces; cancellous bone volume and microarchitecture

a. Young males at 7, 14, 28, and 90 d of HU and 14, 28, and 90 d of recovery from HU

b. Old males at 14 d and 90 d of HU and 14 and 90 d of recovery from HU (still in progress)

c. Young females at 14 d HU

C. Immunohistochemistry staining for osteocyte sclerostin

a. Young males at 14 and 90 d of HU and 14 and 90 d of weightbearing (WB) recovery from HU

b. Old males at 14 d and 90 d of HU and 14 and 90 d of weightbearing recovery from HU (still in progress)

c. Young females at 14 d HU

Summary of key findings (organized under original hypotheses): H1: Increases in Scl-IHC in osteocytes of cortical mid-shaft bone will be observed by 4 days of HLS in mid-shaft cortical bone, preceding a decline in formation indices. These increases will remain high throughout the period of HLS.

H2: Scl-IHC in metaphyseal bone osteocytes (cortical shell and cancellous core) will follow a similar pattern as in mid-shaft osteocytes, but increases will be delayed till 7 days of HLS or later.

Information in NASA Human Research Program (HRP) meeting 2016 poster: At 14 d of HU there was no detectable elevation of % sclerostin-positive osteocytes in any of 3 bone compartments analyzed (mid-shaft cortical bone, cortical shell and cancellous core of femur metaphysis) in young male rats. An unusual 3-fold elevation of % osteoid surface (our one bone formation index) was observed at this time point. We did observe a small decline over 14 d HU in total/integral and cancellous volumetric bone mineral density (vBMD) at the proximal tibia metaphysis (by pQCT measures). [NASA HRP 2016 poster:] We did observe ~50% increase in %sclerostin-positive osteocytes at 90 d HU but only in cancellous bone compartment. At this same time point, % osteoid surface remained elevated above weightbearing controls. The same % deficit in total/integral and cancellous volumetric bone mineral density (vBMD) at the proximal tibia metaphysis that was observed after 14 d HU was observed at 90 d HU, suggesting a plateauing of bone loss in the latter stages of this prolonged unloading period.

H3: During the initial weightbearing recovery period, Scl-IHC will decline relative to peak HLS values in all bone compartments, preceding a local increase in formation indices. Scl-IHC and indices of bone formation will approach aging control values after 90 days of recovery.

Answering this hypothesis awaits completion of sclerostin protein immunostaining osteocytes in recovery samples.

H4: Relative changes in Scl-IHC and indices of bone formation, and the timing thereof, during HLS and recovery in young female rats will not be different from those observed in young male rats.

Information in NASA HRP 2017 poster: There were no differences in the prevalence of %sclerostin-positive osteocytes between male and female rats after 14 d HU. However, females did not exhibit the increase in % osteoid surface as observed in males at this time point (no change vs. WB controls); they also exhibited a 25% increase in %osteoclast surface. Interestingly, pQCT scans could not detect declines in total/integral and cancellous vBMD at the proximal tibia metaphysis in these female rats as was observed in males. Histological (and likely more precise evaluation) of cancellous bone volume revealed a significant decline in females but not males.

H5: Relative changes in Scl-IHC and indices of bone formation will be smaller in these older male rats (9-mo-old) with unloading and a return to weightbearing, but the relationship between magnitude of change in Scl-IHC and bone formation will not be altered by aging.

Answering this hypothesis awaits completion of sclerostin immunostaining in older male rat samples.

Information in Texas Chapter of American College of Sports Medicine (ACSM) 2017 poster: Older (9-month-old) male rats do not experience the significant declines (12-26%) in total/integral and cancellous vBMD at the proximal tibia, nor the decline in cancellous bone volume and trabecular number (by histomorphometry) at the proximal tibia metaphysis that were observed in young (3-month-old) rats after 14 days of hindlimb unloading. This could result, in part, from the fact that older male weightbearing controls have much lower values for these parameters than do the young controls, suggesting there is a lower inherent limit to these values.

Bibliography Type: Description: (Last Updated: 05/28/2021)  Show Cumulative Bibliography Listing
 
Abstracts for Journals and Proceedings Metzger CE, Bloomfield SA. "Altered osteocyte sclerostin with 90 days of hindlimb unloading." Poster Presentation at 2016 NASA Human Research Program Investigators’ Workshop, Galveston, TX, February 8-11, 2016.

2016 NASA Human Research Program Investigators’ Workshop, Galveston, TX, February 8-11, 2016. , Feb-2016

Abstracts for Journals and Proceedings Metzger CE, Bloomfield SA. "Altered osteocyte sclerostin with 90 days of hindlimb unloading." Poster Presentation at 2017 NASA Human Research Program Investigators’ Workshop, Galveston, TX, January 23-26, 2017.

2017 NASA Human Research Program Investigators’ Workshop, Galveston, TX, January 23-26, 2017. , Jan-2017

Abstracts for Journals and Proceedings Anderson AM, Metzger CE, Bloomfield SA. "Disuse–induced bone loss is impacted by age." 2017 meeting of the Texas Chapter of the American College of Sports Medicine, Waco, TX, February 16-17, 2017.

2017 meeting of the Texas Chapter of the American College of Sports Medicine, Waco, TX, February 16-17, 2017. , Feb-2017

Project Title:  Sclerostin's Role in Regulating Bone Formation during Long-term Simulated Microgravity and Subsequent Recovery Reduce
Fiscal Year: FY 2016 
Division: Human Research 
Research Discipline/Element:
HRP HHC:Human Health Countermeasures
Start Date: 10/06/2014  
End Date: 08/31/2017  
Task Last Updated: 10/12/2015 
Download report in PDF pdf
Principal Investigator/Affiliation:   Bloomfield, Susan A. Ph.D. / Texas A&M University 
Address:  Department of Health & Kinesiology 
400 Harvey Mitchell Pkwy, Suite 300 
College Station , TX 77843-4375 
Email: sbloom@tamu.edu 
Phone: 979-845-2871  
Congressional District: 17 
Web:  
Organization Type: UNIVERSITY 
Organization Name: Texas A&M University 
Joint Agency:  
Comments:  
Project Information: Grant/Contract No. NNX15AB05G 
Responsible Center: NASA JSC 
Grant Monitor: Norsk, Peter  
Center Contact:  
Peter.norsk@nasa.gov 
Solicitation / Funding Source: 2013 HERO NNJ13ZSA002N-Crew Health (FLAGSHIP & NSBRI) 
Grant/Contract No.: NNX15AB05G 
Project Type: GROUND 
Flight Program:  
TechPort: No 
No. of Post Docs:
No. of PhD Candidates:
No. of Master's Candidates:
No. of Bachelor's Candidates:
No. of PhD Degrees:
No. of Master's Degrees:
No. of Bachelor's Degrees:
Human Research Program Elements: (1) HHC:Human Health Countermeasures
Human Research Program Risks: (1) Osteo:Risk Of Early Onset Osteoporosis Due To Spaceflight (No longer used, July 2020)
Human Research Program Gaps: (1) Osteo04:We do not know the contribution of each risk factor on bone loss and recovery of bone strength, and which factors are the best targets for countermeasure application (IRP Rev E)
Flight Assignment/Project Notes: NOTE: Extended to 8/31/2017 per NSSC information (Ed., 1/24/17)

NOTE: Extended to 10/05/2016 per NSSC information (Ed., 10/28/15)

Task Description: The tissue sharing opportunity outlined in Appendix A, Item B (“Cerebral Spinal Fluid Production/Absorption....”) offers an exciting chance to study the evolution of changes over 90 days of hindlimb suspension (HLS) in a rodent model. Few laboratories have the capability or expertise to carry out HLS for such a long period; the impact of this experiment will be multiplied many-fold with piggyback projects making strategic use of other tissues harvested from these animals. This proposal focuses on tracking the evolution of changes in a protein important to bone integrity called sclerostin over the course of 90 days of unloading and then during the 90-day recovery phase. Importantly, we will also track alterations in the key physiological function sclerostin regulates in bone: osteoblast activity resulting in the formation of new bone.

Sclerostin is produced by osteocytes, the bone cells embedded in bone matrix and the key sensors of loading/unloading; it works to inhibit the Wnt-Beta catenin signaling pathway in osteoblasts, which normally stimulates bone formation activity. Most studies to date document an increase in osteocyte’s sclerostin expression with unloading, which provides the mechanism for the suppressed bone formation seen with HLS on Earth and, presumably, with microgravity exposure. A recent study examining the impact of a novel therapeutic agent (sclerostin antibody) on mice flown on STS-135 yielded very positive findings, suggesting that manipulating sclerostin expression could be an important therapeutic tool to augment the usual exercise countermeasures employed by astronauts. Hence it becomes critical, before any such systemic therapy is considered, to understand clearly the relationship between sclerostin expression and the functionally important outcome (bone formation activity) in multiple bone sites.

Because there is evidence that Sost, the gene encoding the protein sclerostin, is expressed differently in mid-shaft vs metaphyseal bone, we will assess sclerostin expression and histomorphometric measures of bone formation in 3 different bone compartments for each bone: mid-shaft cortical bone, cancellous bone of the metaphysis and the metaphyseal cortical shell. We propose to first study these outcomes in paired tibiae or femurs (unloaded bone) and in normally loaded humeri. With the availability of female mice in the parent study’s 2nd specific aim, we can then assess if there are gender differences in this response. Recently published data on spaceflown mice document an increase in bone volume in calvarial bone, raising the intriguing possibility that fluid shifts during spaceflight may increase fluid pressures in the rodent brain compartment, providing a mechanical loading of sorts to the skull. Hence, a third specific aim of our proposal, pending verification that calvarial bone can be made available, will assess sclerostin expression and bone formation variables in this unique site to test this hypothesis. At the end of one year’s intensive effort, then, we will have gained a much more clear picture of how this important regulatory molecule is altered by unloading and whether sclerostin antibody does present a viable therapeutic tool for maintaining bone integrity on long-duration missions. In addition, we will gain important fundamental knowledge about the time course of sclerostin expression and its relationship to bone formation rate with alterations in mechanical loading.

Research Impact/Earth Benefits: Phase III clinical trials testing the efficacy of sclerostin antibody (Scl-AB) are in progress, focusing on the value of this agent in reversing aging-related bone loss and osteoporosis. It will be very useful to have data on a physiologically relevant mammalian model (skeletally mature rats) yielding information on the efficacy of Scl-AB for bone loss due to prolonged disuse. This applies to individuals subjected to prolonged bed rest (complicated orthopedic injuries, frail elderly with severe illness) or to conditions like spinal cord injury or even stroke (if significant muscle paralysis is involved). Additionally, this study will provide a sex comparison, so we will have preliminary clues as to whether women might respond similarly as do men to this potent anabolic treatment.

Task Progress & Bibliography Information FY2016 
Task Progress: The first major accomplishment was the acquisition, installation and training with an upgraded OsteoMeasure image analysis system in the Bloomfield Bone Biology Laboratory, completed by November 15, 2014. The improved resolution of the digital camera and a digitizing screen that allows tracing right on the screen itself has resulted in improved speed on analyses of histomorphometry and of immunostaining sections. Both of these methods are central to the purpose of this project.

We received our first shipment of bones from the parent protocol at UC-Davis in early April of 2015 (n ~ 43) from young adult male rats, including samples from animals sacrificed after 7, 14, 28, and 90 days of hindlimb unloading, as well as after 28 days of weight-bearing recovery. Our revised protocol submitted in August, 2014, after negotiations with Dr. Peter Norsk and the parent protocol Principal Investigator (PI) (C Fuller), described proposed work we would perform on the tibial bone samples targeted to our laboratory for analysis. Our first task was to run ex vivo pQCT scans to quantitate bone structural changes on both the metaphysis, a site very sensitive to disuse, and the mid-shaft bone. Outcomes here include volumetric bone mineral density (vBMD), bone mineral content, and cross-sectional geometry (e.g., bone area, cortical thickness, marrow area). Once these were complete, the proximal half of one tibia was prepared histologically for embedding in hard plastic in order for us to perform standard static histomorphometry on the proximal tibial metaphysis. Quantitating the extent of surfaces covered by newly formed bone matrix (osteoid) and by osteoclasts (bone resorbing cells) provides useful information on the balance between bone forming and bone resorbing activity. [Because the parent protocol PI was reticent to add more procedures to an already complicated protocol, there was no injection of fluorochrome labels in these rats during the experiments at UC-Davis, which disallows determination of bone formation rate.]

Summary of results: To date, 2-month old male rats exposed to hindlimb unloading (HLU) demonstrate the expected reductions in vBMD at the proximal tibia metaphysis, as compared to age-matched controls at both 14 and 90 days of HLU. The trend of bone loss appears to remain consistent from 7 days through to recovery (28 days of weight bearing recovery following 90 days of HU). Our histomorphometry results thus far are not consistent with these structural changes in bone described by the pQCT data. Despite the bone loss, there is a paradoxical increase in osteoid surface (newly formed bone matrix yet to be mineralized) at both 14 days and 90 days with the suggestion of similar trends at both 28 days HLU and 28 days of recovery. Likewise, there is a decrease in osteoclast surface (a measure of bone resorption) in HLU at 14 days with no different between HLU and CC at 90 days. Limitations of our current work with this study include the low animal numbers at all time points except 14 days and 90 days, making it difficult to draw firm conclusions of the time course of HLU changes. These preliminary data will be presented at the NASA Human Research Program (HRP) Investigator Workshop in February 2016.

Bibliography Type: Description: (Last Updated: 05/28/2021)  Show Cumulative Bibliography Listing
 
 None in FY 2016
Project Title:  Sclerostin's Role in Regulating Bone Formation during Long-term Simulated Microgravity and Subsequent Recovery Reduce
Fiscal Year: FY 2015 
Division: Human Research 
Research Discipline/Element:
HRP HHC:Human Health Countermeasures
Start Date: 10/06/2014  
End Date: 10/05/2015  
Task Last Updated: 11/21/2014 
Download report in PDF pdf
Principal Investigator/Affiliation:   Bloomfield, Susan A. Ph.D. / Texas A&M University 
Address:  Department of Health & Kinesiology 
400 Harvey Mitchell Pkwy, Suite 300 
College Station , TX 77843-4375 
Email: sbloom@tamu.edu 
Phone: 979-845-2871  
Congressional District: 17 
Web:  
Organization Type: UNIVERSITY 
Organization Name: Texas A&M University 
Joint Agency:  
Comments:  
Project Information: Grant/Contract No. NNX15AB05G 
Responsible Center: NASA JSC 
Grant Monitor: Norsk, Peter  
Center Contact:  
Peter.norsk@nasa.gov 
Solicitation / Funding Source: 2013 HERO NNJ13ZSA002N-Crew Health (FLAGSHIP & NSBRI) 
Grant/Contract No.: NNX15AB05G 
Project Type: GROUND 
Flight Program:  
TechPort: No 
No. of Post Docs:  
No. of PhD Candidates:  
No. of Master's Candidates:  
No. of Bachelor's Candidates:  
No. of PhD Degrees:  
No. of Master's Degrees:  
No. of Bachelor's Degrees:  
Human Research Program Elements: (1) HHC:Human Health Countermeasures
Human Research Program Risks: (1) Osteo:Risk Of Early Onset Osteoporosis Due To Spaceflight (No longer used, July 2020)
Human Research Program Gaps: (1) Osteo04:We do not know the contribution of each risk factor on bone loss and recovery of bone strength, and which factors are the best targets for countermeasure application (IRP Rev E)
Task Description: The tissue sharing opportunity outlined in Appendix A, Item B (“Cerebral Spinal Fluid Production/Absorption....”) offers an exciting chance to study the evolution of changes over 90 days of hindlimb suspension (HLS) in a rodent model. Few laboratories have the capability or expertise to carry out HLS for such a long period; the impact of this experiment will be multiplied many-fold with piggyback projects making strategic use of other tissues harvested from these animals. This proposal focuses on tracking the evolution of changes in a protein important to bone integrity called sclerostin over the course of 90 days of unloading and then during the 90-day recovery phase. Importantly, we will also track alterations in the key physiological function sclerostin regulates in bone: osteoblast activity resulting in the formation of new bone.

Sclerostin is produced by osteocytes, the bone cells embedded in bone matrix and the key sensors of loading/unloading; it works to inhibit the Wnt- Beta catenin signaling pathway in osteoblasts, which normally stimulates bone formation activity. Most studies to date document an increase in osteocyte’s sclerostin expression with unloading, which provides the mechanism for the suppressed bone formation seen with HLS on Earth and, presumably, with microgravity exposure. A recent study examining the impact of a novel therapeutic agent (sclerostin antibody) on mice flown on STS-135 yielded very positive findings, suggesting that manipulating sclerostin expression could be an important therapeutic tool to augment the usual exercise countermeasures employed by astronauts. Hence it becomes critical, before any such systemic therapy is considered, to understand clearly the relationship between sclerostin expression and the functionally important outcome (bone formation activity) in multiple bone sites.

Because there is evidence that Sost, the gene encoding the protein sclerostin, is expressed differently in mid-shaft vs metaphyseal bone, we will assess sclerostin expression and histomorphometric measures of bone formation in 3 different bone compartments for each bone: mid-shaft cortical bone, cancellous bone of the metaphysis and the metaphyseal cortical shell. We propose to first study these outcomes in paired tibiae or femurs (unloaded bone) and in normally loaded humeri. With the availability of female mice in the parent study’s 2nd specific aim, we can then assess if there are gender differences in this response. Recently published data on spaceflown mice document an increase in bone volume in calvarial bone, raising the intriguing possibility that fluid shifts during spaceflight may increase fluid pressures in the rodent brain compartment, providing a mechanical loading of sorts to the skull. Hence, a third specific aim of our proposal, pending verification that calvarial bone can be made available, will assess sclerostin expression and bone formation variables in this unique site to test this hypothesis. At the end of one year’s intensive effort, then, we will have gained a much more clear picture of how this important regulatory molecule is altered by unloading and whether sclerostin antibody does present a viable therapeutic tool for maintaining bone integrity on long-duration missions. In addition, we will gain important fundamental knowledge about the time course of sclerostin expression and its relationship to bone formation rate with alterations in mechanical loading.

Research Impact/Earth Benefits: 0

Task Progress & Bibliography Information FY2015 
Task Progress: New project for FY2015.

Bibliography Type: Description: (Last Updated: 05/28/2021)  Show Cumulative Bibliography Listing
 
 None in FY 2015