Bone microarchitecture and local gene expression in elderly men with osteoporotic hip fractures

Bone ◽  
2012 ◽  
Vol 51 (6) ◽  
pp. S13
Author(s):  
U. Föger-Samwald ◽  
J.M. Patsch ◽  
J. Deutschmann ◽  
L. Hornek ◽  
S. Salem ◽  
...  
2014 ◽  
Author(s):  
Ursula Foger-Samwald ◽  
Alaghebandan Afarin ◽  
Janina Patsch ◽  
Doris Schamall ◽  
Sylvia Salem ◽  
...  

2018 ◽  
Vol 125 (5) ◽  
pp. 1536-1554 ◽  
Author(s):  
Mette Flindt Heisterberg ◽  
Jesper L. Andersen ◽  
Peter Schjerling ◽  
Alberte Lund ◽  
Simone Dalskov ◽  
...  

Our purpose here was to investigate the potential of blocking the angiotensin II type I receptor (AT1R) on the hypertrophy response of elderly human skeletal muscle to 4 mo of heavy-resistance exercise training. Fifty-eight healthy elderly men (+65 yr) were randomized into three groups, consuming either AT1R blocker (losartan, 100 mg/day) or placebo for 4 mo. Two groups performed resistance training (RT) and were treated with either losartan or placebo, and one group did not train but was treated with losartan. Quadriceps muscle biopsies, MR scans, and strength tests were performed at baseline and after 8 and 16 wk. Biopsies were sectioned for immunohistochemistry to determine the number of satellite cells, capillaries, fiber type distribution, and fiber area. Gene expression levels of myostatin, connective tissue, and myogenic signaling pathways were determined by real-time RT-PCR. Four months of heavy-resistance training led in both training groups to expected improvements in quadriceps (∼3–4%) and vastus lateralis (∼5–6%), cross-sectional area, and type II fiber area (∼10–18%), as well as dynamic (∼13%) and isometric (∼19%) quadriceps peak force, but with absolutely no effect of losartan on these outcomes. Furthermore, no changes were seen in satellite cell number with training, and most gene targets failed to show any changes induced by training or losartan treatment. We conclude that there does not appear to be any effect of AT1R blocking in elderly men during 4 mo of resistance training. Therefore, we do not find any support for using AT1R blockers for promoting muscle adaptation to training in humans. NEW & NOTEWORTHY Animal studies have suggested that blocking angiotensin II type I receptor (AT1R) enhances muscle regeneration and prevents disuse atrophy, but studies in humans are limited. Focusing on hypertrophy, satellite cells, and gene expression, we found that AT1R blocking did not result in any greater responses with 4 mo of resistance training. These results do not support previous findings and question the value of blocking AT1R in the context of preserving aging human muscle.


2005 ◽  
Vol 37 (Supplement) ◽  
pp. S242
Author(s):  
Masashi Kamioka ◽  
Haruka Murakami ◽  
Kouki Takahashi ◽  
Naoki Mukai ◽  
Syunpei Miyakawa ◽  
...  

2005 ◽  
Vol 37 (Supplement) ◽  
pp. S243
Author(s):  
Shlomit Radom-Aizik ◽  
Shlomo Hayek ◽  
Gidi Rechavi ◽  
Ninette Amariglio ◽  
Hillel Halkin ◽  
...  

2010 ◽  
Vol 22 (8) ◽  
pp. 2385-2393 ◽  
Author(s):  
H.-F. Hwang ◽  
H.-D. Lee ◽  
H.-H. Huang ◽  
C.-Y. Chen ◽  
M.-R. Lin

2005 ◽  
Vol 37 (Supplement) ◽  
pp. S242
Author(s):  
Masashi Kamioka ◽  
Haruka Murakami ◽  
Kouki Takahashi ◽  
Naoki Mukai ◽  
Syunpei Miyakawa ◽  
...  

Author(s):  
Xi Shao ◽  
Yongqing Yang ◽  
Zhifen Tan ◽  
Yuanjun Ding ◽  
Erping Luo ◽  
...  

Type 2 diabetes mellitus (T2DM) results in compromised bone microstructure and quality, and subsequently increased risks of fractures. However, it still lacks safe and effective approaches resisting T2DM bone fragility. Pulsed electromagnetic fields (PEMF) exposure has proven to be effective in accelerating fracture healing and attenuating osteopenia/osteoporosis induced by estrogen deficiency. Nevertheless, whether and how PEMF resist T2DM-associated bone deterioration remain not fully identified. The KK-Ay mouse was used as the T2DM model. We found that PEMF stimulation with 2 h/day for 8 weeks remarkably improved trabecular bone microarchitecture, decreased cortical bone porosity, and promoted trabecular and cortical bone material properties in KK-Ay mice. PEMF stimulated bone formation in KK-Ay mice, as evidenced by increased serum levels of bone formation (osteocalcin and P1NP), enhanced bone formation rate and increased osteoblast number. PEMF significantly suppressed osteocytic apoptosis and sclerostin expression in KK-Ay mice. PEMF exerted beneficial effects on osteoblast- and osteocyte-related gene expression in the skeleton of KK-Ay mice. Nevertheless, PEMF exerted no effect on serum biomarkers of bone resorption (TRAcP5b and CTX-1), osteoclast number or osteoclast-specific gene expression (TRAP and cathepsin K). PEMF upregulated gene expression of canonical Wnt ligands (including Wnt1, Wnt3a and Wnt10b), but not non-canonical Wnt5a. PEMF also upregulated skeletal protein expression of downstream p-GSK-3β and β-catenin in KK-Ay mice. Moreover, PEMF-induced improvement in bone microstructure, mechanical strength and bone formation in KK-Ay mice was abolished after intragastric administration with the Wnt antagonist ETC-159. Together, our results suggest that PEMF can improve bone microarchitecture and quality by enhancing the biological activities of osteoblasts and osteocytes, which are associated with the activation of the Wnt/β-catenin signaling pathway. PEMF might become an effective countermeasure against T2DM-induced bone deterioration.


2005 ◽  
Vol 37 (10) ◽  
pp. 1680-1696 ◽  
Author(s):  
SHLOMIT RADOM-AIZIK ◽  
SHLOMO HAYEK ◽  
IRIS SHAHAR ◽  
GIDEON RECHAVI ◽  
NAFTALI KAMINSKI ◽  
...  

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