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Osteoporosis: HELP
Articles by Daohong Zhou
Based on 2 articles published since 2010
(Why 2 articles?)
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Between 2010 and 2020, Daohong Zhou wrote the following 2 articles about Osteoporosis.
 
+ Citations + Abstracts
1 Article Elimination of senescent osteoclast progenitors has no effect on the age-associated loss of bone mass in mice. 2019

Kim, Ha-Neui / Chang, Jianhui / Iyer, Srividhya / Han, Li / Campisi, Judith / Manolagas, Stavros C / Zhou, Daohong / Almeida, Maria. ·Division of Endocrinology and Metabolism, Center for Osteoporosis and Metabolic Bone Diseases, University of Arkansas for Medical Sciences, Little Rock, Arkansas. · The Central Arkansas Veterans Healthcare System, Little Rock, Arkansas. · Department of Pharmaceutical Sciences and Winthrop P. Rockefeller Cancer Institute, University of Arkansas for Medical Sciences, Little Rock, Arkansas. · Department of Orthopedic Surgery, University of Arkansas for Medical Sciences, Little Rock, Arkansas. · Buck Institute for Research on Aging, Novato, California. · Lawrence Berkeley National Laboratory, Berkeley, California. · Department of Pharmacodynamics, College of Pharmacy, University of Florida, Gainesville, Florida. ·Aging Cell · Pubmed #30773784.

ABSTRACT: Both an increase in osteoclast and a decrease in osteoblast numbers contribute to skeletal aging. Markers of cellular senescence, including expression of the cyclin inhibitor p16, increase with aging in several bone cell populations. The elimination of p16-expressing cells in old mice, using the INK-ATTAC transgene, increases bone mass indicating that senescent cells contribute to skeletal aging. However, the identity of the senescent cells and the extent to which ablation of p16-expressing cells may prevent skeletal aging remain unknown. Using mice expressing the p16-3MR transgene, we examined whether elimination of p16-expressing cells between 12 and 24 months of age could preserve bone mass; and whether elimination of these cells from 20 to 26 months of age could restore bone mass. The activation of the p16-3MR transgene by ganciclovir (GCV) greatly diminished p16 levels in the brain, liver, and osteoclast progenitors from the bone marrow. The age-related increase in osteoclastogenic potential of myeloid cells was also abrogated by GCV. However, GCV did not alter p16 levels in osteocytes-the most abundant cell type in bone-and had no effect on the skeletal aging of p16-3MR mice. These findings indicate that the p16-3MR transgene does not eliminate senescent osteocytes but it does eliminate senescent osteoclast progenitors and senescent cells in other tissues, as described previously. Elimination of senescent osteoclast progenitors, in and of itself, has no effect on the age-related loss of bone mass. Hence, other senescent cell types, such as osteocytes, must be the seminal culprits.

2 Article DNA damage and senescence in osteoprogenitors expressing Osx1 may cause their decrease with age. 2017

Kim, Ha-Neui / Chang, Jianhui / Shao, Lijian / Han, Li / Iyer, Srividhya / Manolagas, Stavros C / O'Brien, Charles A / Jilka, Robert L / Zhou, Daohong / Almeida, Maria. ·Division of Endocrinology and Metabolism, Center for Osteoporosis and Metabolic Bone Diseases, University of Arkansas for Medical Sciences, Little Rock, AR, USA. · Central Arkansas Veterans Healthcare System, Little Rock, AR, USA. · Department of Pharmaceutical Sciences, University of Arkansas for Medical Sciences, Little Rock, AR, USA. ·Aging Cell · Pubmed #28401730.

ABSTRACT: Age-related bone loss in mice results from a decrease in bone formation and an increase in cortical bone resorption. The former is accounted by a decrease in the number of postmitotic osteoblasts which synthesize the bone matrix and is thought to be the consequence of age-dependent changes in mesenchymal osteoblast progenitors. However, there are no specific markers for these progenitors, and conclusions rely on results from in vitro cultures of mixed cell populations. Moreover, the culprits of such changes remain unknown. Here, we have used Osx1-Cre;TdRFP mice in which osteoprogenitors express the TdRFP fluorescent protein. We report that the number of TdRFP-Osx1 cells, freshly isolated from the bone marrow, declines by more than 50% between 6 and 24 months of age in both female and male mice. Moreover, TdRFP-Osx1 cells from old mice exhibited markers of DNA damage and senescence, such as γH2AX foci, G1 cell cycle arrest, phosphorylation of p53, increased p21