B-cell lymphoma 6 promotes proliferation and survival of trophoblastic cells

Muschol-Steinmetz, Cornelia; Jasmer, Britta; Kreis, Nina-Naomi; Steinhäuser, Kerstin; Ritter, Andreas; Rolle, Udo; Yuan, Juping; Louwen, Frank

doi:10.1080/15384101.2016.1149273

Cited by 26 publications

(24 citation statements)

References 56 publications

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“…Related to this, here we demonstrated that in vivo HIF-1α interference leads to a lower expression of miR-127-3p and, consequently, increased expression of its target gene Bcl6, a transcriptional repressor involved in apoptosis31 and survival regulation32. Previous results of our lab demonstrated that miR127-3p is regulated by HIF-1α during proximal epithelial cell response to ischemia and it is a protector mechanism against renal ischemic injury13.…”

Section: Discussionsupporting

confidence: 76%

HIF-1α induction during reperfusion avoids maladaptive repair after renal ischemia/reperfusion involving miR127-3p

Conde

Giménez-Moyano

Martín-Gómez

et al. 2017

Sci Rep

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Ischemia/reperfusion (I/R) leads to Acute Kidney Injury. HIF-1α is a key factor during organ response to I/R. We previously demonstrated that HIF-1α is induced during renal reperfusion, after ischemia. Here we investigate the role of HIF-1α and the HIF-1α dependent mechanisms in renal repair after ischemia. By interference of HIF-1α in a rat model of renal I/R, we observed loss of expression and mis-localization of e-cadherin and induction of α-SMA, MMP-13, TGFβ, and collagen I. Moreover, we demonstrate that HIF-1α inhibition promotes renal cell infiltrates by inducing IL-1β, TNF-α, MCP-1 and VCAM-1, through NFkB activity. In addition, HIF-1α inhibition induced proximal tubule cells proliferation but it did not induce compensatory apoptosis, both in vivo. In vitro, HIF-1α knockdown in HK2 cells subjected to hypoxia/reoxygenation (H/R) promote cell entry into S phase, correlating with in vivo data. HIF-1α interference leads to downregulation of miR-127-3p and induction of its target gene Bcl6 in vivo. Moreover, modulation of miR-127-3p in HK2 cells subjected to H/R results in EMT regulation: miR127-3p inhibition promote loss of e-cadherin and induction of α-SMA and collagen I. In conclusion, HIF-1α induction during reperfusion is a protector mechanism implicated in a normal renal tissue repair after I/R.

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Section: Discussionsupporting

confidence: 76%

HIF-1α induction during reperfusion avoids maladaptive repair after renal ischemia/reperfusion involving miR127-3p

Conde

Giménez-Moyano

Martín-Gómez

et al. 2017

Sci Rep

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“…Western blot analysis was performed as previously described [53, 63]. Following antibodies were used: Mouse monoclonal antibodies against cyclin B1, Plk1 and p53 (Santa Cruz).…”

Section: Methodsmentioning

confidence: 99%

Impact of Polo-like kinase 1 inhibitors on human adipose tissue-derived mesenchymal stem cells

et al. 2016

Self Cite

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Polo-like kinase 1 (Plk1) has been established as one of the most promising targets for molecular anticancer intervention. In fact, various Plk1 inhibitors have been identified and characterized. While the data derived from the bench are prospective, the clinical outcomes are less encouraging by showing modest efficacy. One of the explanations for this discrepancy could be unintendedly targeting of non-malignant cells by Plk1 inhibitors. In this work, we have addressed the effect of Plk1 inhibition in adipose tissue-derived mesenchymal stem cells (ASCs). We show that both visceral and subcutaneous ASCs display monopolar spindles, reduced viability and strong apoptosis induction upon treatment with BI 2536 and BI 6727, the Plk1 kinase domain inhibitors, and with Poloxin, the regulatory Polo-box domain inhibitor. While Poloxin triggers quickly apoptosis, BI 2536 and BI 6727 result in mitotic arrest in ASCs. Importantly, survived ASCs exhibit DNA damage and a pronounced senescent phenotype. In addition, Plk1 inhibition impairs ASCs' motility and homing ability. These results show that Plk1 inhibitors target slowly proliferating ASCs, an important population of anti-inflammation and immune modulation. The toxic effects on primary cells like ASCs could be partially responsible for the reported moderate antitumor activity in patients treated with Plk1 inhibitors.

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“…Western blot analysis was performed as reported (Muschol-Steinmetz et al, 2016;Steinhauser et al, 2017), using mouse monoclonal antibodies against cyclin B1 (#sc-752) and b-actin (#sc-47778) from Santa Cruz Biotechnology (Heidelberg).…”

Section: Depolymerization Assays Sag Stimulation Cell Viability Anmentioning

confidence: 99%

Primary cilia are dysfunctional in obese adipose-derived mesenchymal stem cells

Ritter

Friemel

Kreis

et al. 2018

Geburtshilfe Und Frauenheilkunde

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Adipose-derived mesenchymal stem cells (ASCs) have crucial functions, but their roles in obesity are not well defined. We show here that ASCs from obese individuals have defective primary cilia, which are shortened and unable to properly respond to stimuli. Impaired cilia compromise ASC functionalities. Exposure to obesity-related hypoxia and cytokines shortens cilia of lean ASCs. Like obese ASCs, lean ASCs treated with interleukin-6 are deficient in the Hedgehog pathway, and their differentiation capability is associated with increased ciliary disassembly genes like AURKA. Interestingly, inhibition of Aurora A or its downstream target the histone deacetylase 6 rescues the cilium length and function of obese ASCs. This work highlights a mechanism whereby defective cilia render ASCs dysfunctional, resulting in diseased adipose tissue. Impaired cilia in ASCs may be a key event in the pathogenesis of obesity, and its correction might provide an alternative strategy for combating obesity and its associated diseases.

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B-cell lymphoma 6 promotes proliferation and survival of trophoblastic cells

Cited by 26 publications

References 56 publications

HIF-1α induction during reperfusion avoids maladaptive repair after renal ischemia/reperfusion involving miR127-3p

HIF-1α induction during reperfusion avoids maladaptive repair after renal ischemia/reperfusion involving miR127-3p

Impact of Polo-like kinase 1 inhibitors on human adipose tissue-derived mesenchymal stem cells

Primary cilia are dysfunctional in obese adipose-derived mesenchymal stem cells

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