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1.
AIM: To observe the mechanisms of RhoA on vascular reactivity following hemorrhagic shock (HS) in rats. METHODS: The superior mesenteric artery (SMA) in rats subjected to hemorrhagic shock was adopted to assay the vascular reactivity via observing the contraction initiated by norepinephrine (NE) with isolated organ perfusion system. Meanwhile, the effects of Rho kinase, myosin light chain phosphatase (MLCP), myosin light chain kinase (MLCK) on RhoA regulating vascular reactivity were observed. The effects of RhoA agonist U-46619 and inhibitor C3 enzyme on the activities of Rho kianse, MLCP, MLCK and phosphorylation of MLC20 in the vascular smooth muscle cells (VSMC) with hypoxia were also measured. RESULTS: As compared to control group, the cumulative dose-response curves of SMA to NE at 2 h after shock shifted to the right, the maximal contractions (Emax) of NE was significantly decreased. RhoA agonist U-46619 increased the vascular reactivity in the late period of shock. C3 enzyme abolished U-46619 induced the increase in the contractile response of SMA to NE. Rho kinase inhibitor Y-27632 decreased U-46619-induced the increase in the vascular reactivity, MLCP inhibitor calyculin further promoted the increase in the vascular reactivity. However, MLCK inhibitor had no effect on the U-46619-induced change of vascular reactivity. After hypoxia, the activities of Rho kinase and MLCK, and the level of MLC20 phosphorylation were decreased, MLCP activity was increased. RhoA agonist U-46619 increased the activity of Rho kinase and phosphorylation of MLC20, decreased the activity of MLCP, but had no effects on MLCK activity. CONCLUSION: RhoA plays an important role in the regulation of vascular reactivity following shock. The mechanism is closely related to regulating the activities of Rho kinase and MLCP, and increasing the phosphorylation of MLC20 in VSMC.  相似文献   

2.
AIM:The present study was to investigate the roles of protein kinase C α and δ isoforms (PKC-α, δ) in arginine vasopressin (AVP) improved contractile response of vascular smooth muscle cells (VSMC) to norepinephrine (NE) after hypoxia and its relations to myosin light chain (MLC20) phosphorylation, myosin light chain phosphatase (MLCP) and myosin light chain kinase (MLCK) activity.METHODS: Primary cultures of VSMC were obtained from the superior mesenteric artery (SMA) of rats by explanting technique and the cells in third to fifth passage were used in the study. The effects of PKC-α and δ antagonists on AVP induced contractile response of VSMC to NE after 1.5 h hypoxia were observed by measuring the ratio of accumulative infiltration of fluorescent isothiocyanate-conjugated bovine serum albumin with transwell, and their effect on the activity of MLCP/MLCK in VSMC was assayed by enzymatic catalysis. At the same time, with the SMA from hemorrhagic shock rats (30 mmHg for 2 h), the effects of PKC α and δ isoforms in the regulation of AVP on MLC20 phosphorylation of SMA after shock were observed by Western blotting.RESULTS: G 6976 (5×10-6 mol/L, PKC-α isoform inhibitor) significantly antagonized AVP (5×10-10 mol/L)-induced increase in the contractile response of VSMC to NE after hypoxia, and rottlerin (10-5 mol/L, PKC-δ isoform inhibitor) also partly inhibited this effect. Hypoxia resulted in a significant increase in MLCP activity, with a decrease in MLCK activity of VSMC, and at the same time, the MLC20 phosphorylation of SMA following hemorrhagic shock was significantly decreased. AVP inhibited the activity of MLCP and increased the phosphorylation of MLC20, which was inhibited by G 6976, while rottlerin treatment only showed a slightly inhibitory effect. AVP and PKC-α, δ inhibitor had no significant influence on MLCK activity.CONCLUSION:AVP up-regulates vascular reactivity and calcium sensitivity of VSMC possibly through inhibiting the activity of MLCP and increasing the phosphorylation of MLC20 by PKC-α isoform.  相似文献   

3.
AIM:To explore the signal transduction pathways of calcium-sensing receptor(CaSR) that mediates hypoxia-induced proliferation of rat pulmonary artery smooth muscle cells(PASMCs). METHODS:The expression of cyclin D1 and phosphorylated protein kinase B(p-Akt) was analyzed by Western blotting. Cell proliferation was tested using a BrdU incorporation assay, and cell cycle analysis was carried out using a flow cytometric assay. RESULTS:Hypoxia significantly increased the expression of cyclin D1 and p-Akt, the BrdU incorporation and the cell proliferation index. GdCl3, an agonist of CaSR, amplified the effect of hypoxia. LY294002,a PI3K inhibitor, decreased the up-regulation of cyclin D1 expression and the BrdU incorporation, and also inhibited the increase in the cell proliferation index induced by hypoxia and GdCl3 in PASMCs. CONCLUSION: The CaSR mediates hypoxia-induced proliferation of rat PASMCs through PI3K pathways.  相似文献   

4.
AIM:To explore the role of four-and-a-half LIM domain 1 (FHL1) in the proliferation and migration of rat distal pulmonary arterial smooth muscle cells (PASMCs) stimulated by cigarette smoke extract (CSE). METHODS:Rat distal PASMCs were isolated and primarily cultured. The cells were divided into 6 groups: blank control group, negative transfection group, FHL1 siRNA transfection group, CSE group, CSE + negative transfection group and CSE + FHL1 siRNA transfection group. The mRNA and protein expression of FHL1 was detected by real-time PCR and Western blotting, respectively. Cell proliferation and migration were determined by CCK-8 and Transwell assays, respectively. RESULTS:CSE promoted the proliferation and migration of PASMCs, and increased the expression of FHL1 protein (P<0.01), but did not change the expression of FHL1 mRNA (P>0.05). FHL1 siRNA transfection attenuated the proliferation and migration of PASMCs induced by CSE (P<0.01). CONCLUSION: FHL1 protein is involved in CSE-induced proliferation and migration of rat PASMCs.  相似文献   

5.
AIM: To investigate the role of nuclear factor kappa B (NF-κB) signaling in the changes of permeability in brain-derived microvascular endothelial (bEnd.3) cells induced by lipopolysaccharide (LPS).METHODS: The bEnd.3 cells were randomly divided into 3 groups: bEnd.3 group, bEnd.3/vector group and bEnd.3/muIκBα group. The cells in the latter 2 groups were transfected with pcDNA3.1hygro and DNMu-IκBα (a dominant-negative mutant of IκB) plasmids, respectively. All the cells were exposed to LPS. The activity of NF-κB, monolayer barrier integrity and F-actin distribution were detected by luciferase reporter assay, transendothelial electrical resistance (TEER) assay and rhodamine-phalloidin staining, respectively. The expression of tight junction proteins (ZO-1 and claudin-5) and phosphorylation of myosin light chain (MLC) were determined using Western blotting.RESULTS: In bEnd.3 group and bEnd.3/vector group, the NF-κB activity began to increase obviously as early as 0.5 h after pretreatment with LPS. LPS decreased TEER, and induced F-actin rearrangement and ZO-1 down-regulation in 3 h. Incubation of the cells with LPS for 12 h induced the most significant disruptive effects on the permeability and tight junctions. Moreover, high expression of phosphorylated MLC accompanied with the early damages of tight junctions was observed. However, these destabilizing alterations were suppressed in bEnd.3/muIκBα group by the inhibition of NF-κB activity.CONCLUSION: LPS induces hyperpermeability in brain microvascular endothelial cells. The functions of NF-κB signaling are related to influencing disruptions of tight junctions by regulating the phosphorylation of MLC.  相似文献   

6.
AIM:To study the effect of farrerol (Far) on nicotine-induced proliferation of rat pulmonary smooth muscle cells (PASMCs), and further to explore its relationship with voltage-dependent potassium channels (Kv) 1.5 and Kv2.1. METHODS:Firstly, the effect of nicotine on the proliferation of PASMCs was detected by cell counting method, and the optimal concentration of nicotine was selected. Primary cultured PASMCs were randomly divided into 5 groups:normal control group, nicotine (1 μmol/L)group, nicotine (1 μmol/L) + Far (10-6 mol/L, 10-5 mol/L and 10-4 mol/L) Far group. The activity of caspase-3 was measured by apoptosis kit, the cell viability was measured by CCK-8 assay, the apoptotic rate was analyzed by flow cytometry. The expression of Kv1.5 and Kv2.1, and apoptosis-related factors Bcl-2 and Bax at mRNA and protein levels was determined by RT-qPCR and Western blot respectively. RESULTS:Nicotine at 1 μmol/L increased the number of PASMCs to the maximum extent (P<0.01). Nicotine at 1 μmol/L significantly reduced the caspase-3 activity and enhanced the cell viability of the PASMCs (P<0.01). Farrerol at 10-6~10-4 mol/L eliminated the effect of PASMCs induced by nicotine in a concentration dependent manner. Compared with control group, nicotine at 1 μmol/L significantly increased the proliferation and inhibited the apoptotic rate of rat PASMCs (P<0.01). The apoptotic rate of PASMCs in farrerol intervention group was significantly higher than that in nicotine group (P<0.01). Nicotine at 1 μmol/L significantly inhibited the expression of Kv1.5, Kv2.1 and Bax but increased the expression of Bcl-2 in PASMCs (P<0.01). Farrerol at 10-5 mol/L obviously inhibited the effect of PASMCs induced by nicotine. CONCLUSION:Farrerol eliminates nicotine-induced inhibition of caspase-3 and Bax, and enhancement of Bcl-2 in PASMCs by enhancing Kv1.5 and Kv2.1 expression.  相似文献   

7.
AIM: To investigate the effects of bradykinin (BK) on the proliferation of pulmonary artery smooth muscle cells (PASMCs) induced by transforming growth factor beta 1 (TGF-β1) and its possible mechanisms. METHODS: Primary porcine PASMCs were isolated, cultured and identified, and the cells at passages 2~6 were used in this study. The viability of PASMCs was determined by Cell Counting Kit-8 assay. The protein expression of phosphatidylinositol 3-kinase (PI3K), phosphorylated Akt (p-Akt) and phosphorylated extracellular signal-regulated kinase 1/2 (p-ERK1/2) was detected by Western blotting. RESULTS: TGF-β1 promoted the proliferation of PASMCs in a dose-dependent manner (P<005). BK significantly inhibited the proliferation of PASMCs induced by TGF-β1 (P<005), and attenuated the elevated expression of PI3K, p-Akt and p-ERK1/2 proteins (P<005). HOE-140, a BK type 2 receptor (B2R) inhibitor, reversed the effects of BK (P<005). CONCLUSION: BK inhibits TGF-β1-induced proliferation of PASMCs, which may be associated with inactivation of PI3K/Akt and ERK1/2 signaling pathways.  相似文献   

8.
AIM: To explore the role of calcium-sensing receptor (CaSR) in rat pulmonary artery smooth muscle cells (PASMCs) and its effect on hypoxia-induced proliferation of PASMCs. METHODS: The expression and distribution of CaSRs were detected by Western blotting and immunofluorescence observation. The intracellular concentration of free calcium ([Ca]i) was determined by confocal laser scanning microscopy. The cell viability was analyzed by MTT assay. The expression of PCNA and CaSRs was determined by Western blotting. RESULTS: CaSR protein was expressed in rat PASMCs. Hypoxia significantly increased the expression of CaSR and PCNA,[Ca]i and the cell viability. GdCl3 (an agonist of CaSR) or NPS2390 (an antagonist of CaSR) amplified or weakened the effect of hypoxia, respectively.CONCLUSION: CaSR is expressed in rat PASMCs. The activation of CaSR is involved in the proliferation of PASMCs induced by hypoxia.  相似文献   

9.
AIM: To investigate the role of autophagy in the injury of human umbilical vein endothelial cells (HUVECs) induced by ursolic acid (UA). METHODS: HUVECs were cultured in vitro with UA at various concentrations for 36 h and the proliferation inhibitory rate of HUVECs was determined by MTT method. The change of ultrastructure was observed under transmission electronic microscope (TEM). The autophagy was observed using fluorescent microscope by monodansylcadaverin (MDC) staining. The protein level and mRNA expression of microtubule-associated protein light chain 3(LC3) and Beclin-1 were detected by Western blotting and RT-PCR, respectively. Cell apoptotic rate was measured by flow cytometry analysis. RESULTS: UA at various concentrations showed significantly dose-dependent inhibitory effect on the proliferation of HUVECs. Autophagy was induced in HUVECs treated with UA as detected by MDC staining and TEM. The protein level and mRNA expression of LC3 and Beclin-1 in HUVECs were significantly increased following the treatment with UA, which was also in a time-dependent manner. Compared with UA group, addition of 3-methyladenine(3-MA) inhibited the increase in autophagic vacuoles and exacerbated the apoptosis. CONCLUSION: Autophagy shows protective effect on the proliferation inhibition of HUVECs induced by UA and the proliferation inhibition can be enhanced by the autophagy inhibitor 3-MA. 3-MA may enhance the apoptotic rate of HUVECs induced by UA.  相似文献   

10.
AIM: To observe the effects of She Xiang Bao Xin Wan (SXBXW) of Chinese patent medicine on the proliferation of primary cultured vascular smooth muscle cells (VSMCs) from human umbilical artery and stimulated by endothelin-1 (ET-1) in vitro. METHODS: The proliferation cell models of primary cultured VSMCs were established by ET-1 stimulation. Six groups in the experiment were divided into control group; ET-1 group; ET-1+SXBXW 0.25 g/L; ET-1+SXBXW 0.5 g/L; ET-1+SXBXW 1.0 g/L and ET-1+SXBXW 2.0 g/L groups, respectively. The proliferation induced by ET-1 and the suppression mediated by SXBXW on VSMCs were measured by MTT method. The inhibitory rate and the cytotoxicity of SXBXW were detected by lactate dehydrogenase colorimetry and trypan blue exclusion tests. The effect of ET-1 and SXBXW on the cell proliferation cycle was analyzed by flow cytometry. RESULTS: Compared to control group, ET-1 significantly enhanced the proliferation of VSMCs (P<0.01). However, a certain dose of SXBXW inhibited effectively the proliferation of VSMCs induced by ET-1 in a dose-dependent manner (P<0.01). Meanwhile, SXBXW showed no influenced on both the number of living cells and the release of lactate dehydrogenase, although it inhibited the proliferation of VSMCs, indicating that SXBXW was no cytotoxicitic effect on VSMCs. ET-1 enhanced the proliferation of VSMCs by means of promoting the transition of the cell cycle from G1 phase to S phase. However SXBXW significantly inhibited the proliferation mediated by ET-1. CONCLUSION: SXBXW plays the role in suppressing VSMCs proliferation induced by ET-1. The mechanism may be involved in blocking the cell cycle from G1 phase into S phase.  相似文献   

11.
AIM: To observe the effect of ginsenoside Rb1 on the proliferation and the expression of serotonin transporter (SERT), 5-hydroxytryptamine 1B receptor (5HT1BR) in rat pulmonary artery smooth muscle cells (PASMCs) under hypoxia condition and the relationship with Rho/Rho-kinase signal pathway.METHODS: PASMCs were isolated from the adult male SD rats and primarily cultured. The subcultured cells from the 4th generation to the 6th generation were harvested and divided into normal group, and hypoxia group, different concentrations of Rb1 incubation groups treated with 50, 100 and 200 mg/L ginsenoside Rb1 under hypoxia (HR50, HR100 and HR200 groups, respectively). The viability of the PASMCs was measured by CCK-8 assay. BrdU positive cells were determined using flow cytometry. The expression of serotonin transporter and 5HT1BR at mRNA and protein levels was detected by RT-PCR and Western blot, respectively. The PASMCs were randomly divided into normal group, hypoxia group, HR200 group and hypoxia+Y-27632 incubation group (HY group). The mRNA expression of Rho-kinase and phosphorylated myosin phosphatase target subunit 1 (p-MYPT1) protein level were investigated by RT-PCR and Western blot, respectively.RESULTS: Compared with normal group, the proliferation of PASMCs in hypoxia group was significantly increased (P<0.01). The cell viability and the expression of SERT and 5HT1BR at mRNA and protein levels in all different concentrations of Rb1 groups were obviously decreased compared with hypoxia group (P<0.05). The mRNA expression of Rho-kinase and protein level of p-MYPT1 were markedly decreased in HR200 group, and no significant difference compared with HY group was observed (P<0.01).CONCLUSION: Treatment with ginsenoside Rb1 might prevent hypoxia-induced proliferation of PASMCs and over-expression of SERT and 5HT1BR through inhibiting the Rho/Rho-kinase pathway.  相似文献   

12.
AIM: To investigate the regulatory mechanism of Cx40 and Cx43 on endothelium-dependent vascular contractile reactivity and calcium sensitivity following hemorrhagic shock in rats. METHODS: The rat superior mesenteric arteries (SMAs) were isolated and vascular rings were prepared. Transfection of Cx40 and Cx43 antisense oligodeoxyribonucleotide (Cx40 and Cx43AODN) was conducted to block the expressions of Cx40 and Cx43 in SMAs. The changes of contractile response, calcium sensitivity, the activity of myosin light chain phosphatase (MLCP) and myosin light chain kinase (MLCK), 20kD myosin light chain (MLC20) phosphorylation in hypoxia treated SMA were observed. RESULTS: Cx40AODN decreased the activity of MLCP, increased the MLC20 phosphorylation, by which Cx40AODN improved the calcium sensitivity and the contractile response of SMA. Cx43AODN increased the activity of MLCP, reduced the MLC20 phosphorylation, by which Cx43AODN depressed the calcium sensitivity and the contractile response of SMA. No effect of Cx40 and Cx43AODN on the MLCK′s activity of SMA was observed. CONCLUSION: The mechanism that Cx40 and Cx43 regulates endothelium-dependent vaso-contractile responses following hemorrhagic shock may be mainly through regulating the activity of MLCP and MLC20 phosphorylation in vascular smooth muscle cells.  相似文献   

13.
Myosin light chain kinase (MLCK) activates the regulatory light chain of myosin II, and the phosphorylated myosin light chain leads to actomyosin contractile activity, as well as the cell contraction and increasing intercellular gap, which finally results in endothelial barrier dysfunction. MLCK-dependent hyperpermeability occurs in response to multiple cell signaling molecules and signaling pathways, including Ca2+, Src, PKC, NO, cGMP and mitogen activated protein kinases (MAPK). In this review, different mechanisms of endothelial hyperpermeability mediated by MLCK are discussed.  相似文献   

14.
CAO Xue-wu  GAO Yu-qi 《园艺学报》2006,22(3):452-455
AIM: To determine the effect of agmatine on the proliferation of pulmonary artery smooth muscle cells (PASMCs) induced by hypoxia. METHODS: Primary culture of rat PASMCs was prepared from adult male Wistar rat pulmonary artery by the method of tissue block anchorage. PASMCs were divided into two groups: control group and agmatine-treated group. The activity of LDH in the medium was measured by chromatometry. ［3H］-TdR incorporation was measured by liquid scintillation counting. The cell cycle was measured by flow cytometry, and the PCNA content was measured by image analysis. RESULTS: Agmatine did not exert significant effect on the activity of LDH in the medium, but significantly decreased the ［3H］-TdR incorporation and PCNA content of PASMCs. Agmatine significantly decreased the cell ratio of G2/M phase and increased the cell ratio of G0/G1 phase. With the increment of the concentration of agmatine, ［3H］-TdR incorporation was significantly decreased. CONCLUSION: Agmatine has no significant cytotoxic effect on PASMCs and agmatine dose-dependently inhibits the proliferation of rat PASMCs induced by hypoxia.  相似文献   

15.
AIM：To investigate the expression of volume-activated chloride channel (CLC3) in rat pulmonary artery smooth muscle cells (PASMCs) treated with hypoxia and hypercapnia and its relationship with MAPK pathway. METHODS：The method of enzyme digestion was used to isolate the PASMCs in male SD rat for cell primary culture. The cells were identified by immunofluorescence cytochemical method with mouse anti-rat α-smooth muscle actin antibody. The rat model of hypoxia and hypercapnia was established. The protein expression of CLC3 was detected by Western blotting. The mRNA expression of CLC3 was determined by RT-PCR. RESULTS：Compared with control group, the mRNA and protein expression of CLC3 in PASMCs was significantly raised in hypoxia and hypercapnia group. Compared with hypoxic and hypercapnic group, the expression of CLC3 was significantly reduced in ERK inhibitor U0126+ hypoxia and hypercapnia group, and was up-regulated in p38 inhibitor SB203580+ hypoxia and hypercapnia group. p38 activator anisomycin significantly decreased the expression of CLC3 at mRNA and protein levels in hypoxia and hypercapnia group. CONCLUSION：The expression of CLC3 at mRNA and protein levels in PASMCs increases under hypoxia and hypercapnia conditions. The ERK1/2 pathway mediates CLC3 expression in PASMCs induced by hypoxia and hypercapnia. Activation of p38 MAPK pathway down-regulates the expression of CLC3 at mRNA and protein levels induced by hypoxia and hypercapnia.  相似文献   

16.
HONG Yan  ZHAO Mei 《园艺学报》2018,34(10):1848-1854
AIM: The present study aimed to investigate the role of microRNA-339 miR-339 in the proliferation of pulmonary artery smooth muscle cells (PASMCs). METHODS: After treating with angiotensin Ⅱ of different concentrations for 48 h, miR-339 mimic and miR-339 inhibitor were transfected into PASMCs, respectively. CCK-8 assay and viable cell counting were performed to determine cell proliferation. The expression levels of miR-339 and PCNA mRNA were measured by RT-qPCR. The protein levels were detected by Western blot. The interaction between miR-339 and insulin-like growth factor 2 mRNA-binding protein 1(IGF2BP1) was confirmed by luciferase reporter assay. RESULTS: Angiotensin Ⅱ concentration-dependently increased cell proliferation and mRNA expression of PCNA, and decreased miR-339 expression in the PASMCs. Over-expression of miR-339 inhibited cell proliferation and mRNA expression of PCNA in the PASMCs, while mutation of miR-339 promoted cell proliferation and mRNA expression of PCNA in the PASMCs. In addition, miR-339 inhibited cell proliferation in angiotensin Ⅱ-treated PASMCs. Bioinformatics analysis showed that miR-339 targeted the IGF2BP1 3'-UTR, which was confirmed by luciferase reporter assay, and miR-339 negatively regulated the expression of IGF2BP1 in the PASMCs. More importantly, over-expression of IGF2BP1 attenuated the inhibitory effects of miR-339 on cell proliferation and mRNA expression of PCNA in the PASMCs. miR-399 over-expression suppressed phosphorylated p38 protein level but not p38 protein level. CONCLUSION: miR-339 suppresses anti-proliferative effects in PASMCs partly via regulating IGF2BP1 and p38 MAPK signaling pathway.  相似文献   

17.
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18.
AIM：To investigate the effect of c-Myc inhibitor 10058-F4 on human chronic myeloid leukemia (CML) K562 cells and imatinib-resistant K562/G cells. METHODS：The protein expression of c-Myc was detected by Western blotting. Cell proliferation was evaluated by MTT assay and colony formation assay. PI staining was used to determine the cell cycle distribution. Annexin V-PI staining was applied for apoptosis detection. RESULTS：Imatinib-resistant K562/G cells displayed lower sensitivity to imatinib than K562 cells with high expression of c-Myc. Treatment with specific c-Myc inhibitor 10058-F4 inhibited the cell proliferation in a dose- and time-dependent manner, and K562/G displayed more sensitivity to 10058-F4 than K562 cells. 10058-F4 also induced cell cycle arrest in G0/G1 phase and induced apoptotic cell death in the 2 cells. Importantly, 10058-F4 suppressed the colony formation ability in K562 and K562/G cells. CONCLUSION：c-Myc is a novel target to overcome imatinib-induced drug resistance, and c-Myc inhibitor provides a new approach in CML therapy.  相似文献   

19.
AIM: To investigate the effect of SCH900776, an inhibitor of checkpoint kinase 1 (CHK1), on the proliferation and migration abilities of human glioma U251 cells.METHODS: The cell viability was detected by MTT assay, and cell proliferation was determined by cell colony formation assay. Cell cycle distribution was analyzed by flow cytometry. Wound healing assay was used to determine the cell migration ability. The protein levels were determined by Western blot.RESULTS: SCH900776 inhibited the growth of U251 cells in a dose-dependent manner (P<0.05). SCH900776 treatment substantially induced U251 cell cycle arrest in S and G2/M phases by decreasing the level of cell division cycle protein 2 (Cdc2) and p-Cdc2. Moreover, SCH900776 inhibited the cell migration. Western blot results indicated that SCH900776 increased the phosphorylation level of p38 MAPK and inhibited the activation of Akt.CONCLUSION: SCH900776 inhibits the proliferation and migration abilities in human U251 cells by promoting the phosphorylation of p38 MAPK and suppressing the activation of Akt.  相似文献   

20.
AIM：To investigate the effects of voltage-dependent K＋ channel 1.5 (Kv1.5) on the proliferation and apoptosis of rat pulmonary artery smooth muscle cells (PASMCs) under hypoxia+hypercapnia condition and the relationship with mitogen-activated protein kinase(MAPK) signal pathway. METHODS：The PASMCs isolated from the male SD rat were cultured under hypoxia+hypercapnia condition, and randomly divided into normal group (N group), hypoxia+hypercapnia group (HH group), hypoxia+hypercapnia+DMSO incubation group (HD group), hypoxia+hypercapnia+U0126 (an extracellular signal-regulated kinase 1/2 inhibitor) incubation group (HU group), hypoxia+hypercapnia+SB203580 (a p38 mitogen-activated protein kinase inhibitor) incubation group (HS group), and hypoxia+hypercapnia+anisomycin (an agonist of MAPK) incubation group (HA group). Cell Counting Kit-8 was used to detect the cell viability. The protein expression of Kv1.5, PCNA and Bax was detected by Western blotting. RESULTS：Compared with N group, the cell viability and PCNA protein expression in HH group and HD group were significantly raised (P<001), but Kv1.5 and Bax proteins were significantly decreased (P<0.01). No difference between HH group and HD group was observed (P>005). Compared with HD group, the cell viability and PCNA protein expression in HU group, HS group and HA group were decreased (P<0.05 or P<0.01), but Kv1.5 protein and Bax protein were raised (P<0.01), with the most significant changes in HA group. CONCLUSION：The regulation of Kv1.5 to the proliferation and apoptosis of PASMCs under hypoxia+hypercapnia condition might have a relationship with the activation of MAPK signal pathway.  相似文献   

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