Title : Adenosine A2A Receptor in Bone Marrow-Derived Cells Mediated Macrophages M2 Polarization via PPARγ-P65 Pathway in Chronic Hypoperfusion Situation.

Pub. Date : 2021

PMID : 35046793






11 Functional Relationships(s)
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1 Under low-glucose and hypoxic conditions, CGS21680 treatment promoted macrophage M2 polarization, increased the expression of PPARgamma, P65, and interleukin-10 (IL-10) and suppressed the expression of tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta). 2-(4-(2-carboxyethyl)phenethylamino)-5'-N-ethylcarboxamidoadenosine peroxisome proliferator activated receptor gamma Mus musculus
2 Under low-glucose and hypoxic conditions, CGS21680 treatment promoted macrophage M2 polarization, increased the expression of PPARgamma, P65, and interleukin-10 (IL-10) and suppressed the expression of tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta). 2-(4-(2-carboxyethyl)phenethylamino)-5'-N-ethylcarboxamidoadenosine interleukin 10 Mus musculus
3 Under low-glucose and hypoxic conditions, CGS21680 treatment promoted macrophage M2 polarization, increased the expression of PPARgamma, P65, and interleukin-10 (IL-10) and suppressed the expression of tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta). 2-(4-(2-carboxyethyl)phenethylamino)-5'-N-ethylcarboxamidoadenosine interleukin 10 Mus musculus
4 Under low-glucose and hypoxic conditions, CGS21680 treatment promoted macrophage M2 polarization, increased the expression of PPARgamma, P65, and interleukin-10 (IL-10) and suppressed the expression of tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta). 2-(4-(2-carboxyethyl)phenethylamino)-5'-N-ethylcarboxamidoadenosine tumor necrosis factor Mus musculus
5 Under low-glucose and hypoxic conditions, CGS21680 treatment promoted macrophage M2 polarization, increased the expression of PPARgamma, P65, and interleukin-10 (IL-10) and suppressed the expression of tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta). 2-(4-(2-carboxyethyl)phenethylamino)-5'-N-ethylcarboxamidoadenosine tumor necrosis factor Mus musculus
6 Under low-glucose and hypoxic conditions, CGS21680 treatment promoted macrophage M2 polarization, increased the expression of PPARgamma, P65, and interleukin-10 (IL-10) and suppressed the expression of tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta). 2-(4-(2-carboxyethyl)phenethylamino)-5'-N-ethylcarboxamidoadenosine interleukin 1 beta Mus musculus
7 Under low-glucose and hypoxic conditions, CGS21680 treatment promoted macrophage M2 polarization, increased the expression of PPARgamma, P65, and interleukin-10 (IL-10) and suppressed the expression of tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta). 2-(4-(2-carboxyethyl)phenethylamino)-5'-N-ethylcarboxamidoadenosine interleukin 1 alpha Mus musculus
8 The CGS21680-induced upregulation of P65 and IL-10 was abolished in macrophages upon PPARgamma knockdown. 2-(4-(2-carboxyethyl)phenethylamino)-5'-N-ethylcarboxamidoadenosine interleukin 10 Mus musculus
9 The CGS21680-induced upregulation of P65 and IL-10 was abolished in macrophages upon PPARgamma knockdown. 2-(4-(2-carboxyethyl)phenethylamino)-5'-N-ethylcarboxamidoadenosine peroxisome proliferator activated receptor gamma Mus musculus
10 The downregulation of TNF-alpha and IL-1beta by CGS21680 was less affected by PPARgamma knockdown. 2-(4-(2-carboxyethyl)phenethylamino)-5'-N-ethylcarboxamidoadenosine tumor necrosis factor Mus musculus
11 The downregulation of TNF-alpha and IL-1beta by CGS21680 was less affected by PPARgamma knockdown. 2-(4-(2-carboxyethyl)phenethylamino)-5'-N-ethylcarboxamidoadenosine interleukin 1 alpha Mus musculus