Heparanase enhances nerve-growth-factor-induced PC12 cell neuritogenesis via the p38 MAPK pathway

Cui, Heping; Shao, Chenghao; Liu, Qin; Yu, Wenjie; Fang, Jianping; Yu, Weishi; Ali, Amjad; Ding, Kan

doi:10.1042/bj20110167

Cited by 24 publications

(23 citation statements)

References 45 publications

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“…Notably, it is supposed that there are complex relationships between HPSE and p38 MAPK pathway. Previous studies have showed HPSE may enhance three main MAPK members (including p38, ERK and JNK, solely or simultaneously) by phosphorylation 34–36; certain pathophysiology processes induced by HPSE could be mediated after p38 regulation 37,38. In our study, however, the concurrent of HPSE up-regulation and sole p38 activation is a unique feature of HG induction and the mechanism for sole p38 activation is still obscure.…”

Section: Discussioncontrasting

confidence: 51%

High glucose‐induced intestinal epithelial barrier damage is aggravated by syndecan‐1 destruction and heparanase overexpression

Qing

Zhang

Chen

et al. 2015

J Cellular Molecular Medi

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Syndecan-1 (Sdc1) and its endo-beta-d-glucuronidase heparanase (HPSE) are implicated in maintenance of intestinal epithelial barrier (IEB), but their alterations and roles in high-glucose/hyperglycaemia (HG) conditions have not been fully investigated. This study aimed to determine the expression pattern, the possible regulation mechanism of Sdc1 and HPSE in HG conditions, and their potential effects on IEB. Therefore, diabetic mice/cell models were developed, and tissue/serum samples, cell lysate and culture supernatants were harvested. The expression of Sdc1 and HPSE in control, HG and designated interventions groups were detected. Phosphorylations of mitogen-activated protein kinase signalling pathway (MAPK), the expressions of Occludin and ZO-1, and the levels of transepithelial electrical resistance (TEER) were measured and monitored. The results showed that in HG conditions, intestinal tissue and cellular Sdc1 were significantly decreased, but the expression of HPSE, and soluble Sdc1 in serum and culture supernatants were remarkably increased. Such alterations of Sdc1 and HPSE were associated with solely p38 MAPK activation, and were correlated with the reductions of Occludin, ZO-1 and TEER. Heparin (Sdc1 analogue) and SB203580 (a p38 MAPK inhibitor), instead of insulin, alleviated Sdc1 destruction and HPSE overexpression, and effectively prevented against the reductions of tight junctions and the abnormality of intestinal permeability in HG conditions. In conclusion, we confirm the unique alterations of Sdc1 and HPSE in HG conditions, and found their interactions with p38 MAPK activation and IEB. These indicate that Sdc1/HPSE modulation can be viewed as an important complementary treatment for relieving HG-induced gastrointestinal damage.

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Section: Discussioncontrasting

confidence: 51%

High glucose‐induced intestinal epithelial barrier damage is aggravated by syndecan‐1 destruction and heparanase overexpression

Qing

Zhang

Chen

et al. 2015

J Cellular Molecular Medi

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“…As shown in Figure 4A, a p38 MAPK inhibitor SB203580 [26] and a JNK MAPK inhibitor SP600125 [27] suppressed phosphorylation of p38 and JNK, respectively. These results are in accord with recent reports that not only catalytic activities of p38 and JNK but also phosphorylation of these MAPKs by upstream MAPK kinases are inhibited by SB203580 [28–30] and SP600125 [31–33], respectively, under certain conditions. These MAPK inhibitors also suppressed activation of caspase-3/7 induced by the STS treatment (Figure 4B).…”

Section: Resultssupporting

confidence: 93%

The Apoptotic Volume Decrease Is an Upstream Event of MAP Kinase Activation during Staurosporine-Induced Apoptosis in HeLa Cells

Hasegawa

Shimizu

Takahashi

et al. 2012

IJMS

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Persistent cell shrinkage, called apoptotic volume decrease (AVD), is a pivotal event of apoptosis. Activation of the volume-sensitive outwardly rectifying Cl− channel (VSOR) is involved in the AVD induction. On the other hand, activation of the MAP kinase (MAPK) cascade is also known to play a critical role in apoptosis. In the present study, we investigated the relationship between the AVD induction and the stress-responsive MAPK cascade activation during the apoptosis process induced by staurosporine (STS) in HeLa cells. STS was found to induce AVD within 2–5 min and phosphorylation of c-Jun N-terminal kinase (JNK) and p38 MAPK after over 20–30 min. VSOR blockers suppressed not only STS-induced AVD but also phosphorylation of JNK and p38 as well as activation of caspase-3/7. Moreover, a p38 inhibitor, SB203580, and a JNK inhibitor, SP600125, failed to affect STS-induced AVD, whereas these compounds reduced STS-induced activation of caspase-3/7. Also, treatment with ASK1-specific siRNA suppressed STS-induced caspase-3/7 activation without affecting the AVD induction. Furthermore, sustained osmotic cell shrinkage per se was found to trigger phosphorylation of JNK and p38, caspase activation, and cell death. Thus, it is suggested that activation of p38 and JNK is a downstream event of AVD for the STS-induced apoptosis of HeLa cells.

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“…Previous studies have demonstrated that NGF activates different extracellular and intracellular signaling pathways leading to neurite outgrowth, including the PI3K/Akt and MEK/ERK pathways (18)(19)(20)(21). In the present study, treatment with TFSA led to a significant increase in the phosphorylation of Akt at Ser473.…”

Section: Discussionsupporting

confidence: 59%

Tenuifoliside A promotes neurite outgrowth in PC12 cells via the PI3K/AKT and MEK/ERK/CREB signaling pathways

Liu

Wang

Lü

2015

Molecular Medicine Reports

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Abstract. Previous studies have demonstrated the neuroprotective effect of tenuifoliside A (TFSA) on corticosterone-induced neuron damage in SH-SY5Y cells, however, the effect of TFSA on the promotion of neurite outgrowth remains to be elucidated. PC12 cells were treated with TFSA or nerve growth factor, and the levels of proteins were evaluated by western blotting. In addition, for pharmacological experiments, inhibitors of the PD98059 mitogen-activated protein kinase kinase (MEK) and phosphatidylinositol 3-kinase (PI3K; LY294002) were added into the culture medium. The present study demonstrated that TFSA significantly increased the percentage of neurite-bearing cells and promoted neurite extension in PC12 cells. In addition, TFSA-treated PC12 cells also expressed increased levels of the 43 kD growth-associated protein (GAP-43) neural marker, comparable to those in nerve growth factor-treated cells. The present study also demonstrated that TFSA enhanced the phosphorylation of extracellular signal-regulated kinase (ERK) and Akt, which are important signaling molecules involved in neural differentiation in PC12 cells. Co-treatment of the PC12 cells with the PD98059 MEK inhibitor and LY294002 PI3K inhibitor inhibited the neurite outgrowth induced by TFSA. In addition, treatment with TFSA also promoted the phosphorylation of cyclic AMP response element-binding protein (CREB), which was inhibited completely by treatment with PD98059. In conclusion, the results of the present study demonstrated that TFSA induces neurite extension of PC12 cells and suggested that activation of the MEK/ERK/CREB and PI3K/Akt signaling pathways is involved in this process.

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Heparanase enhances nerve-growth-factor-induced PC12 cell neuritogenesis via the p38 MAPK pathway

Cited by 24 publications

References 45 publications

High glucose‐induced intestinal epithelial barrier damage is aggravated by syndecan‐1 destruction and heparanase overexpression

High glucose‐induced intestinal epithelial barrier damage is aggravated by syndecan‐1 destruction and heparanase overexpression

The Apoptotic Volume Decrease Is an Upstream Event of MAP Kinase Activation during Staurosporine-Induced Apoptosis in HeLa Cells

Tenuifoliside A promotes neurite outgrowth in PC12 cells via the PI3K/AKT and MEK/ERK/CREB signaling pathways

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