Key result
Activation of angiotensin II type 1 receptor suppressed and activation of angiotensin II type 2 receptor enhanced the expression of markers of hypertrophic differentiation in chondrocytes.
Why the study?
Does activation of AT1R and AT2R modulate hypertrophic differentiation in ATDC5 chondrocytes?
Does activation of AT1R and AT2R modulate hypertrophic differentiation in ATDC5 chondrocytes?
In vitro activation of AT1R suppresses, while AT2R enhances, the hypertrophic differentiation of chondrocytes.
Answers are grounded in this paper and cite their sources.
Too preliminary for clinical translation; leaves open AT1R/AT2R modulation of chondrocyte hypertrophy in vivo.
A local tissue-specific renin-angiotensin system (local RAS) has been identified in many organs. However, no report has described the role of a local RAS in the hypertrophic differentiation of chondrocytes. To examine the role of a local RAS in the hypertrophic differentiation, we activated angiotensin II type 1 receptor (AT1R) and angiotensin II type 2 receptor (AT2R) separately in the cell line ATDC5, which involves differentiation from mesenchymal stem cells to hypertrophic chondrocytes. Activation of AT1R suppressed and activation of AT2R enhanced the expression of markers of hypertrophic differentiation, including type X collagen, matrix metalloproteinase 13 and runt-related transcription factor 2.
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Tsukamoto et al. (2013) studied Hypertrophic differentiation of chondrocytes. Angiotensin II with Olmesartan (AT1R inhibitor) or PD123319 (AT2R inhibitor) vs. Control (PBS alone) was evaluated on Expression of markers of hypertrophic differentiation (type X collagen, MMP13, Runx2) (p=<0.05). Activation of angiotensin II type 1 receptor suppressed and activation of angiotensin II type 2 receptor enhanced the expression of markers of hypertrophic differentiation in chondrocytes.
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