Peroxisome proliferator-activated receptor gamma (PPARγ): Is the genomic activity the only answer?

Luconi, Michaela; Cantini, Giulia; Serio, Mario

doi:10.1016/j.steroids.2009.10.012

Cited by 86 publications

(79 citation statements)

References 88 publications

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“…Previous reports have revealed that the transcriptional activity of PPAR␥2 is modulated by phosphorylation, sumoylation, ubiquitylation, and nitration (41). Phosphorylation of PPAR␥2 is presumed to be the most significant negative posttranscriptional regulator among them (42).…”

Section: Discussionmentioning

confidence: 99%

Low Intensity Pulsed Ultrasound (LIPUS) Influences the Multilineage Differentiation of Mesenchymal Stem and Progenitor Cell Lines through ROCK-Cot/Tpl2-MEK-ERK Signaling Pathway

Kusuyama

Bandow

Shamoto

et al. 2014

Journal of Biological Chemistry

119

107

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Background: Low intensity pulsed ultrasound (LIPUS) is a mechanical stimulus clinically used to promote bone fracture healing. Results: LIPUS suppresses adipogenesis and promotes osteogenesis of mesenchyme stem/progenitor cell lines by inhibiting PPAR␥2 through ROCK-Cot/Tpl2-MEK-ERK pathway. Conclusion: LIPUS influences multilineage differentiation of mesenchymal stem and progenitor cells. Significance: LIPUS may be a new clinical approach to chronic bone metabolic disorders, including osteoporosis.

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Section: Discussionmentioning

confidence: 99%

Low Intensity Pulsed Ultrasound (LIPUS) Influences the Multilineage Differentiation of Mesenchymal Stem and Progenitor Cell Lines through ROCK-Cot/Tpl2-MEK-ERK Signaling Pathway

Kusuyama

Bandow

Shamoto

et al. 2014

Journal of Biological Chemistry

119

107

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“…In our work, a compensatory increase in PPARγ gene expression was observed in adipocytes in comparison with pre-adipocytes and treated adipocytes. Furthermore, the activity of PPARγ can be nely tuned through integration of diverse phosphorylation events [33,34]. In this regard, a downward trend in PPARγ protein levels in cells treated with telmisartan for 6 hours in comparison with the untreated group.…”

Section: Discussionmentioning

confidence: 99%

Telmisartan-induced eNOS gene expression is partially independent of its PPAR-gamma agonist property

Esparragón¹,

Pérez²

2012

CIM

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Purpose: Telmisartan, an angiotensin II receptor blocker (ARB), also acts as an activator of peroxisome proliferator-activated receptor-gamma (PPAR-gamma; PPAR-γ). Several studies have explored the PPAR-γ-endothelial nitric oxide synthase (eNOS) pathway associated with improvement of endothelial function by telmisartan. e ability of telmisartan to induce gene expression and protein level of eNOS and PPARγ in adipocytes was investigated.Methods: Expression of aP2, PPARγ, eNOS and iNOS genes were measured using the quantitative real-time polymerase chain reaction. e changes, at the protein level, were explored by Western blot, which evaluated the native and phosphorylated eNOS forms, eNOS-Ser 1177 and eNOS-r 495 .Results: Adipocytes, exposed to telmisartan, exhibited an increase in PPARγ gene expression but a decrease in protein level. Nonetheless, a er the exposure to telmisartan, eNOS-Ser 1177 phosphorylation, associated with eNOS activity increment, reached its highest value while eNOS-r 495 phosphorylation, involved in the inhibition of eNOS activity, showed its lowest value.Conclusion: e results suggest that telmisartan preserves eNOS activity via a mechanism that is partially independent of the PPARγ-eNOS pathway in adipocytes.

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“…Indeed, DNA binding was assessed as a measure of PPARg activation in all the reports studying the functions of PPARs in platelets without exception (Akbiyik et al, 2004;Ali et al, 2006Ali et al, , 2009aKhanolkar et al, 2008;Ray et al, 2008;Moraes et al, 2010). Fortunately, nongenomic, nontranscriptional activities of PPARg are being uncovered (Bishop-Bailey, 2010;Luconi et al, 2010), and such progress may allow us to elucidate the working mechanism of platelet PPARg.…”

Section: Antiplatelet Effects Of Thiazolidinedionesmentioning

confidence: 99%

AMP-Activated Protein Kinase Mediates the Antiplatelet Effects of the Thiazolidinediones Rosiglitazone and Pioglitazone

et al. 2015

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The thiazolidinedione antidiabetic drugs rosiglitazone and pioglitazone exert antiplatelet effects. Such effects are known to be mediated by the peroxisome proliferator-activated receptor g (PPARg), an acknowledged target of the thiazolidinediones, although the molecular mechanism is elusive. Recently, AMP-activated protein kinase (AMPK) signaling was reported to inhibit platelet aggregation. Because AMPK is another target of the thiazolidinediones, the impact of rosiglitazone and pioglitazone on platelet AMPK and its involvement in aggregation were investigated to assess the contribution of AMPK to the antiplatelet activity of these agents. Treatment with rosiglitazone stimulated both AMPK and PPARg in isolated rat platelets. However, the concentration and the treatment time required for activation were distinct from each other. Indeed, stimulation of AMPK and PPARg were discrete events without any cross-activation in platelets. Activation of AMPK or PPARg by rosiglitazone rendered platelets less responsive to aggregatory stimuli such as collagen, ADP, and thrombin. However, the resultant efficacy caused by activating AMPK was higher than that attributable to PPARg stimulation. Similar results were obtained with pioglitazone. Taken together, rosiglitazone and pioglitazone inhibit platelet aggregation by activating AMPK. AMPK functions as a potential target of rosiglitazone and pioglitazone for their antiplatelet activity, although the in vivo or clinical relevance remains to be assessed.

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Peroxisome proliferator-activated receptor gamma (PPARγ): Is the genomic activity the only answer?

Cited by 86 publications

References 88 publications

Low Intensity Pulsed Ultrasound (LIPUS) Influences the Multilineage Differentiation of Mesenchymal Stem and Progenitor Cell Lines through ROCK-Cot/Tpl2-MEK-ERK Signaling Pathway

Low Intensity Pulsed Ultrasound (LIPUS) Influences the Multilineage Differentiation of Mesenchymal Stem and Progenitor Cell Lines through ROCK-Cot/Tpl2-MEK-ERK Signaling Pathway

Telmisartan-induced eNOS gene expression is partially independent of its PPAR-gamma agonist property

AMP-Activated Protein Kinase Mediates the Antiplatelet Effects of the Thiazolidinediones Rosiglitazone and Pioglitazone

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