Suppression of matrix metalloproteinase-9 expression in undifferentiated, non-apoptotic keratinocytes is abrogated by the cleavage of poly(ADP-ribose) polymerase-1

Kobayashi, Takashi

doi:10.1007/s10495-011-0650-9

Cited by 7 publications

(4 citation statements)

References 62 publications

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“…Inhibition of caspase suppresses induction of MMP-9 expression (42). Further, as PARP-1 is involved in the transcriptional activation of MMP-9, induction of apoptosis through caspase activation and PARP-1 cleavage results in re-repression of MMP-9 promoter activity (42). In our study, inhibition of both MMP-9 and MMP-13 reduced TM-induced PARP cleavage, but increased viability of Caki-2 cells (Fig.…”

Section: Discussionsupporting

confidence: 54%

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Suppression of tunicamycin-induced CD44v6 ectodomain shedding and apoptosis is correlated with temporal expression patterns of active ADAM10, MMP-9 and MMP-13 proteins in Caki-2 renal carcinoma cells

Kim

Jung

2012

Oncology Reports

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CD44v6 has been shown to coordinate the activation of anti-apoptotic molecules as well as resistance to apoptosis. Here, we investigated CD44v6 ectodomain shedding in Caki-2 human renal carcinoma cells as well as its underlying mechanisms. Exposure of cells to tunicamycin (TM)-induced apoptosis was accompanied by cleavage of caspase-3, PARP-1 and CD44v6 ectodomain. TM-induced apoptosis was also closely associated with endoplasmic reticulum (ER) stress, as shown by increased expression of GRP-78 and CHOP proteins. Furthermore, induction of matrix metallo-proteinase (MMP)-13, MMP-9 and ADAM10 expression was highly stimulated by tunicamycin in a time- and dose-dependent manner. TM-induced PARP-1 cleavage was significantly inhibited by treatment with GM6001 (a broad spectrum MMP inhibitor), MMP-9/-13 inhibitor and GI254023X (specific ADAM10 inhibitor). In addition, inhibition of all examined MMPs resulted in reversal of TM-induced apoptosis as well as increased cell viability. When considering the functional implications of MMP-9 and ADAM10, it is likely that active MMP-9 and ADAM10 help regulate the cellular levels of CD44v6 through cleavage of CD44v6 ectodomain during TM-induced apoptosis of Caki-2 cells. Collectively, these findings suggest that multiple TM-induced MMPs may cooperate to induce apoptosis.

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Section: Discussionsupporting

confidence: 54%

“…3B). Inhibition of caspase suppresses induction of MMP-9 expression (42). Further, as PARP-1 is involved in the transcriptional activation of MMP-9, induction of apoptosis through caspase activation and PARP-1 cleavage results in re-repression of MMP-9 promoter activity (42).…”

Section: Discussionmentioning

confidence: 99%

Suppression of tunicamycin-induced CD44v6 ectodomain shedding and apoptosis is correlated with temporal expression patterns of active ADAM10, MMP-9 and MMP-13 proteins in Caki-2 renal carcinoma cells

Kim

Jung

2012

Oncology Reports

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“…Such mechanism of de-repression by PARP1 cleavage has been described for MMP-9 and Tcirg1 gene promoters, which are inhibited by intact PARP1: PARP1 dependent repression on Tcirg1 is overcome upon RANKL mediated cleavage of PARP1 [29]. Similarly, PARP1 mediated repression MMP-9 gene promoter was relieved in apoptotic cells upon PARP1 cleavage [43]. Increase in HFE expression (Fig.…”

Section: Discussionmentioning

confidence: 79%

Regulation of HFE expression by poly(ADP-ribose) polymerase-1 (PARP1) through an inverted repeat DNA sequence in the distal promoter

Pelham

Jiménez

Rodova

et al. 2013

Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanism

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Hereditary hemochromatosis (HH) is a common autosomal recessive disorder of iron overload among Caucasians of northern European descent. Over 85% of all cases with HH are due to mutations in the hemochromatosis protein (HFE) involved in iron metabolism. Although the importance in iron homeostasis is well recognized, the mechanism of sensing and regulating iron absorption by HFE, especially in the absence of iron response element in its gene, is not fully understood. In this report, we have identified an inverted repeat sequence (ATGGTcttACCTA) within 1700 bp (−1675/+35) of the HFE promoter capable to form cruciform structure that binds PARP1 and strongly represses HFE promoter. Knockdown of PARP1 increases HFE mRNA and protein. Similarly, hemin or FeCl3 treatments resulted in increase in HFE expression by reducing nuclear PARP1 pool via its apoptosis induced cleavage, leading to upregulation of the iron regulatory hormone hepcidin mRNA. Thus, PARP1 binding to the inverted repeat sequence on the HFE promoter may serve as a novel iron sensing mechanism as increased iron level can trigger PARP1 cleavage and relief of HFE transcriptional repression.

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“…expression of adhesion molecules (von Lukowicz et al 2008), transcriptional regulation of cyclooxygenase-2 (Lin et al 2011), transforming growth factor-b1 (TGF-b1) receptor (Sterling et al 2006), syndecan-4 (Lacal et al 2009), NF-kB (Kauppinen et al 2013), SMAD3 (Huang et al 2011), sex determining region Y-Box-2 (Musard et al 2001) and E-cadherin (McPhee et al 2008), which are essential during embryo implantation (Nakamura et al 2004, San et al 2004, Jha et al 2006, Lin et al 2006, St-Louis et al 2010. Furthermore, cell differentiation, cell proliferation (Lei et al 2009, Kaloglu & Onarlioglu 2010, Macdonald et al 2011, Afshar et al 2012) and the tissue remodelling process also take place in the uterus (Fazleabas & Strakova 2002, Rosario et al 2003, Kaloglu & Onarlioglu 2010, and can be influenced by PARP1 (Pagano et al 2007, Kobayashi 2011. In endometrial carcinoma, PARP1 can regulate the progesterone receptor (PR; Ghabreau et al 2004), suggesting the involvement of PARP1 in ovarian steroid signalling.…”

Section: Introductionmentioning

confidence: 99%

PARP1 during embryo implantation and its upregulation by oestradiol in mice

Joshi¹,

Mahfooz²,

Maurya³

et al. 2014

Reproduction

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Pregnancy requires successful implantation of an embryo, which occurs during a restricted period defined as 'receptivity of the endometrium' and is influenced by the ovarian steroids progesterone and oestradiol. The role of poly(ADP-ribose)polymerase-1 (PARP1) in apoptosis is well established. However, it is also involved in cell differentiation, proliferation and tissue remodelling. Previous studies have described the presence of PARP in the uterus, but its exact role in embryo implantation is not yet elucidated. Hence, in this study, we studied the expression of PARP1 in the uterus during embryo implantation and decidualisation, and its regulation by ovarian steroids. Our results show upregulation of the native form of PARP1 (w116 kDa) in the cytosolic and nuclear compartments of implantation and non-implantation sites at day 5 (0500 h), followed by downregulation at day 5 (1000 h), during the embryo implantation period. The transcript level of Parp1 was also augmented during day 5 (0500 h). Inhibition of PARP1 activity by the drug EB-47 decreased the number of embryo implantation sites and blastocysts at day 5 (1000 h). Further, cleavage of native PARP1 was due to the activity of caspase-3 during the peri-implantation stage (day 5 (0500 h)), and is also required for embryo implantation, as inhibition of its activity compromised blastocyst implantation. The native (w116 kDa) and cleaved (w89 kDa) forms of PARP1 were both elevated during decidualisation of the uterus. Furthermore, the expression level of PARP1 in the uterus was found to be under the control of the hormone oestrogen. Our results clearly demonstrate that PARP1 participates in the process of embryo implantation.

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Suppression of matrix metalloproteinase-9 expression in undifferentiated, non-apoptotic keratinocytes is abrogated by the cleavage of poly(ADP-ribose) polymerase-1

Cited by 7 publications

References 62 publications

Suppression of tunicamycin-induced CD44v6 ectodomain shedding and apoptosis is correlated with temporal expression patterns of active ADAM10, MMP-9 and MMP-13 proteins in Caki-2 renal carcinoma cells

Suppression of tunicamycin-induced CD44v6 ectodomain shedding and apoptosis is correlated with temporal expression patterns of active ADAM10, MMP-9 and MMP-13 proteins in Caki-2 renal carcinoma cells

Regulation of HFE expression by poly(ADP-ribose) polymerase-1 (PARP1) through an inverted repeat DNA sequence in the distal promoter

PARP1 during embryo implantation and its upregulation by oestradiol in mice

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