2018
DOI: 10.1002/jbm4.10035
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Abstract: Young, skeletally mature mice lacking Cx43 in osteocytes exhibit increased osteocyte apoptosis and decreased bone strength, resembling the phenotype of old mice. Further, the expression of Cx43 in bone decreases with age, suggesting a contribution of reduced Cx43 levels to the age-related changes in the skeleton. We report herein that Cx43 overexpression in osteocytes achieved by using the DMP1-8kb promoter (Cx43OT mice) attenuates the skeletal cortical, but not trabecular bone phenotype of aged, 14-month-old … Show more

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Cited by 45 publications
(39 citation statements)
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“…Aging and physical inactivity are each associated with a decrease in lacunae that contain osteocytes, loss of directional orientation of lacunae, and the number and length of dendrites that connect through canniculi; all of which would interfere with the detection of strain or fluid-flow shear stress [25][26][27][28]. Connexin43, a gap junction protein involved in mechanotransduction, protects from osteocyte apoptosis, but also decreases with aging [29][30][31][32]. Alternatively, unloading could induce senescence indirectly through the effect of inactivity on reductions in myokines, adverse changes in whole body nutrient trafficking, and the resulting lipid accumulation in both osteoblasts and osteocytes.…”
Section: Osteocyte Senescence and Mechanical Loadingmentioning
confidence: 99%
“…Aging and physical inactivity are each associated with a decrease in lacunae that contain osteocytes, loss of directional orientation of lacunae, and the number and length of dendrites that connect through canniculi; all of which would interfere with the detection of strain or fluid-flow shear stress [25][26][27][28]. Connexin43, a gap junction protein involved in mechanotransduction, protects from osteocyte apoptosis, but also decreases with aging [29][30][31][32]. Alternatively, unloading could induce senescence indirectly through the effect of inactivity on reductions in myokines, adverse changes in whole body nutrient trafficking, and the resulting lipid accumulation in both osteoblasts and osteocytes.…”
Section: Osteocyte Senescence and Mechanical Loadingmentioning
confidence: 99%
“…4-(young, n=10) and 15-month-old mice (middle-aged, n=10) C57BL/6 female mice were obtained from National Institute on Aging (NIA) and received daily intraperitoneal injection of veh (1.7% DMSO) or 100μg/day (young mice) and 110μg/day (middle-aged mice) of AZ (DC Chemicals, Shanghai, P.R., China, cat.# DC8338), to account for body weight differences, for 28 days. We chose these 2 ages to determine the effect of RAGE inhibition at the age in which the mice reach peak bone mass (4 months of age), and later in life (15months of age), in which we showed there is already a significant deterioration, without reaching very low levels of bone mass and strength that might be difficult to reverse (Davis et al, 2018). Mice were assigned an ID number and the age/treatment were recorded in a database.…”
Section: Mice and Treatmentmentioning
confidence: 99%
“…S5), but no other signs of distress were recorded. Young mice received IP injections of calcein (30 mg/kg; Sigma-Aldrich, Saint Louis, MO, USA) and alizarin red (50 mg/kg; Sigma) 7 and 2 days before sacrifice, respectively and aged mice received IP injections of calcein (30 mg/kg; Sigma-Aldrich, Saint Louis, MO, USA) and alizarin red (50 mg/kg; Sigma) 10 and 3 days before sacrifice, respectively, to allow for dynamic histomorphometric measurements (Davis et al, 2018). The longer duration between labels in aged mice was done to help facilitate the differentiation of the two labels given the slower bone formation rate.…”
Section: Mice and Treatmentmentioning
confidence: 99%
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