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Objective To investigate the association between serum Caveolin-1 level and hemorrhagic transformation (HT) in patients with acute ischemic stroke (AIS) after intravenous thrombolysis with alteplase. Methods A total of 124 patients with AIS who underwent intravenous thrombolysis with alteplase in our hospital from June 2020 to November 2021 were enrolled as subjects, and according to the presence or absence of HT, they were divided into HT group with 19 patients and non-HT group with 105 patients. A total of 40 individuals who underwent physical examination during the same period of time were enrolled as control group. Serum Caveolin-1 level was measured and compared between groups, and the HT group and the non-HT group were compared in terms of the clinical indices including sex, age, body mass index, smoking history, hypertension history, diabetes history, coronary heart disease history, atrial fibrillation history, blood pressure on admission, random venous blood glucose on admission, serum low-density lipoprotein on admission, TOAST classification, and baseline NIHSS score. A logistic regression analysis was used to investigate the influencing factors for HT in AIS patients after intravenous thrombolysis with alteplase. Results The HT group and the non-HT group had a significantly higher serum level of Caveolin-1 than the control group on admission (t=10.937,7.873,P

As an important component of transcellular pathway, Caveolae enables the transcellular transport of substances without disrupting cellular homeostasis. In kidney, albumin crosses glomerular filtration barrier (GFB) via Caveolae. Transcellular transport of albumin plays a crucial role in the pathology of proteinuria. Thus the importance of Caveolae cannot be overstated. However, the acting mechanism of Caveolae affecting transcellular albumin transport in kidney and their signaling pathways have remained largely elusive. This review summarized the latest studies on the regulation of Caveolae affecting transcellular albumin transport. Thus elucidating the relevant mechanisms of action and understanding the pathways of influence may provide potential therapeutic targets in the prevention and alleviation of proteinuria

Objective To explore the mechanism of phosphorylation of caveolin1 (Cav1) in neurological injury after cerebral ischemia-reperfusion in rats. Methods The rats were randomly divided into sham group, model group and inhibitor group(PP2). Neurological function was evaluated by modified neurological deficit score (mNSS) neurobehavioral score, cerebral infarction volume was evaluated by triphenyltetrazolium chloride (TTC) staining, histomorphology after cerebral ischemia-reperfusion was evaluated by Nissl staining, and apoptosis of peri-infarcted tissue was detected by Tunel staining. Western blot and immunofluorescence were used to detect the protein expression of p-Cav1, glial fibrillary acidic protein (GFAP) and ion calcium binding junction molecule 1 (Iba1) in the tissue around cerebral infarction. Results Compared with the sham operation group, there were significantly increased mNSS score, volume of cerebral infarction, number of apoptotic cells and expression of p-Cav1, GFAP and Iba1 in the model group,while the number of Nissl corpuscles decreased. The inhibitor PP2 reduced the changes of the above-mentioned indexes and protect the neurological function of rats with cerebral ischemia-reperfusion injury. Conclusions Inhibition of p-Cav1 may improve the neurological function after cerebral ischemia-reperfusion in rats with potential mechanism of inhibiting glial cell activation and interaction.

Objective To investigate the effect of Caveolin 1 up regulating vascular endothelial growth factor (VEGF) expression on lower limb ischemia in diabetic rats and its mechanism. Methods Fifty six SD rats were divided into the sham opera tion group, operation group, operation combined empty tranfection group and operation combined Caveolin 1 transfection group in July 2018, 14 cases in each group. The lower limb ischemia model was established on the basis of diabetic rat model. After transfection of Caveolin 1 gene with adenovirus vector, the gastrocnemius muscle samples were taken on 14, 21 d after operation. Then t he morphology of muscle cells, Caveolin 1 and VEGF expression levels and vascular density were observed. Results The lower limb tissue ischemic situation and movement function on postoperative 14,21 d in the operation combined Caveolin 1 transfection group were significantly better than those in the operation group and operation combined empty transfection group; the morphological arrangement of gastrocnemius muscle cells on postoperative 14, 21 d was basically normal, and the formation and distribution of blood vessels were gradually increased. The expression levels of Caveolin 1 in gastrocnemius muscle on postoperative 14 din the operation combined transfection group was significantly higher than that in the sham operation group, operation group and operation com bined empty transfection group, moreover which on postoperative 21 d were more obvious, and the differences were statistically significant (P<0. 05). Conclusion Caveolin 1 can induce the up regulation of VEGF expression, promote the angiogenesis and improve the limb ischemia. [ABSTRACT FROM AUTHOR]

Objective To investigate the role of caveolin⁃1 (Cav1) in palmitic acid⁃induced survival of pancreatic islet β⁃cell. Methods Cav1⁃deficient NIT⁃1 cells and mouse primary islets were constructed through lentiviral vector transfection. Control⁃shRNA was transfected as a control. After fatty⁃acid⁃free bovine serum albumin (BSA) and palmitic acid (0.5 mmol/L) incubation for 24 and 48 hours, cell viability and apoptosis werecalculated by methylcyclopentadienyl manganese tricarbonylassay and Hoechst33342/propidium iodide (PI) double staining. Real time PCR and Western blot were used to detect the expression of apoptosis⁃associated mRNA and protein. The t test and one-way ANOVA were used for statistical analysis. Results Compared with the control group, the cell survival rate of the palmitic acid treatment group was significantly decreased (0.89±0.10 vs 0.24±0.04, t=13.49, P<0.01), and mRNA and protein expressions of P18 and P19 were up⁃regulated (1.00±0.09 vs 1.30±0.04, 1.00±0.04 vs 1.37±0.13, t= 5.28,4.71, both P<0.05; 0.87±0.04, 1.48±0.05, 1.02±0.06 vs 1.41±0.07, t=16.50, 7.33, both P<0.01); mRNA expression levels of cysteine⁃containing aspartic proteolytic enzymes (Caspase⁃6, Caspase⁃9, and Caspase⁃12) were significantly up⁃regulated (1.00±0.04 vs 1.57±0.08, 1.01±0.15 vs 1.57±0.20, 1.02±0.19 vs 1.57±0.09, t=11.04,3.88, 4.53, all P<0.05), and protein expression of them were also significantly increased (0.86±0.10 vs 1.28±0.11, 0.69±0.01 vs 0.86±0.06, 0.70±0.02 vs 1.18±0.01, t=4.89,4.84, 37.18, all P<0.01). The cell survival rate of Cav1⁃shRNA+palmitic acid group was significantly higher than that of Ctrl⁃shRNA+ palmitic acid group (0.53±0.10 vs 0.26±0.08, t=4.71, P<0.01). The mRNA and protein expression of P19 were all down⁃regulated (1.53±0.18 vs 0.66±0.04, 1.48±0.05 vs 0.70±0.02, t=8.17, 25.09, both P<0.01); mRNA expression levels of Caspase⁃6, Caspase⁃7, Caspase⁃9 and Caspase⁃12 were down⁃regulated (1.82± 0.11 vs 1.03±0.07, 1.43±0.24 vs 0.42±0.15, 1.41±0.22 vs 0.51±0.18, 1.45±0.18 vs 0.42±0.13, t= 5.48-10.49, all P<0.01), and protein expression of them were also down⁃regulated (0.99±0.14 vs 0.63±0.11, 0.90±0.14 vs 0.62±0.04, 0.90±0.02 vs 0.60±0.04, 1.30±0.01 vs 0.65±0.04, t=3.50-27.31, all P<0.01). Conclusion Cav1 deficiency inhibites palmitic acid⁃induced pancreatic β⁃cell apoptosis via regulating Caspase family, and ultimately protects β cell viability. [ABSTRACT FROM AUTHOR]

Objective To study the expression of serum caveolin-1 (Cav-1) in patients with pulmonary hypertension (PAH) associated with chronic obstructive pulmonary disease (COPD), and to analyze its clinical significance. Methods According to whether combined with PAH, a total of 65 stable COPD patients were divided into COPD group [pulmonary systolic blood pressure (PASP) ＜40 mmHg, 35 cases] and COPD-PAH group (PASP ≥40 mmHg, 30 cases). Thirty healthy volunteers who received physical examination in our hospital during the same period were selected as normal control group. Baseline data, blood gas analysis, lung function indicators, and expression levels of Cav-1, IL-6, and TNF - α were compared. The receiver operating characteristic curve (ROC curve) was plotted and the optimal cut-off value for Cav-1 diagnosis of COPD combined with PAH was analyzed. Results The first second forced respiratory volume (FEV1)/forced vital capacity (FVC), FEV1 percentage of predicted value (FEV1%), and oxygen partial pressure [p(O2)] were lower in the COPD-PAH group and the COPD group than those in the control group, and the partial pressure of carbon dioxide [p(CO2)] and PASP were higher than those in the control group (P＜0.01). The p(O2) was lower in the COPD-PAH group than that in the COPD group, and the p(CO2) and PASP were higher than those in the COPD group (P＜0.01). The expression levels of Cav-1 were decreased gradually in the control group, COPD group and COPD-PAH group, while the expression levels of IL- 6 and TNF-α were increased gradually (P＜0.01). For predicting the risk of COPD combined with PAH, the area under the ROC curve was 0.902, the optimal cut-off value was 6.66 ng/ml with a sensitivity of 76.7% and a specificity of 85.7%. Cav-1 was consistent with the PASP results measured by Doppler ultrasound (Kappa value = 0.627). Conclusion The serum expression of Cav-1 is down-regulated in the patients with PAH associated with COPD, and Cav-1 can be a novel serum marker for the diagnosis of PAH associated with COPD. [ABSTRACT FROM AUTHOR]

Objective: To explore relationship between postoperative serum caveolin-1 contents after open reduction and internal fixation and delayed healing of tibial fracture patients., Methods: From April 2018 to June 2020, 134 tibial fracture patients underwent open reduction and internal fixation were included, and divided into delayed healing group and normal healing group according to fracture healing condition. Contents of serum caveolin-1 protein before operation, 1, 4, 8, 12 weeks after operation between two groups were compared. Influencing factors of delayed healing was analyzed by Logistic regression model, and predictive value of serum caveolin-1 protein on delayed healing was analyzed by receiver operating characteristic(ROC) curve., Results: Fracture healing was evaluated at 4 months after fracture, 93 patients healed well and 41 patients delayed heal. At 1, 4, 8 and 12 weeks, content of serum caveolin-1 protein in delayed healing group was lower than that of normal healing group( P <0.05). There were statistical difference in smoking, diabetes, open fracture and Gutlio Ⅲ fracture between delayed healing group and normal healing group( P <0.05). Smoking, diabetes, open fracture, Gustlio Ⅲ fracture, decrease of serum caveolin-1 protein at 4 and 8 weeks after operation were risk factor of delayed healing by Logistic analysis( P <0.05). By ROC curve analysis, content of serum caveolin-1 protein had predictive value for delayed fracture, the best cut-off values were 12.45 ng/ml and 12.52 ng/ml respectively, corresponding sensitivity were 45.34%, 43.90%, and specificity were 80.65% and 87.10% ( P <0.05)., Conclusion: Decrease of serum caveolin-1 protein content at 4 and 8 weeks after open reduction and internal fixation for tibia fracture patients were related with delayed healing. Detection of serum caveolin-1 protein content at 4 and 8 weeks after operation has predictive value for delayed healing.

To explore whether paeonol can play an anti-atherosclerotic role by regulating the expression of aortic caveolin-1 and affecting NF-κB pathway, so as to inhibit the inflammatory response of vascular endothelium in atherosclerotic rats. The atherosclerotic model of rats was induced by high-fat diet and vitamin D&#95;2. The primary culture of vascular endothelial cells(VECs) was carried out by tissue block pre-digestion and adherent method. The injury model of VECs was induced by lipopolysaccharide(LPS), and filipin, a small concave protein inhibitor, was added for control. HE staining was used to observe pathological changes of aorta. TNF-α, IL-6 and VCAM-1 were detected by ELISA. Western blot assay was used to detect the protein expression levels of caveolin-1 and p65 in aorta and VECs. The results showed that as compared with model group, paeonol significantly reduced aortic plaque area and lesion degree in rats, decreased the level of serum TNF-α, IL-6 and VCAM-1 in the rats and enhanced the relative expression level of caveolin-1, decreased p65 expression conversely(P&lt;0.05 or P&lt;0.01). In vitro, as compared to model group, paeonol obviously improved cell morphology, decreased the secretion of TNF-α, IL-6 and VCAM-1 in VECs, increased caveolin-1 expression, and decreased p65 protein expression(P&lt;0.05 or P&lt;0.01). Furthermore, filipin could reverse the effect of paeonol on expression of inflammatory factors and proteins(P&lt;0.05 or P&lt;0.01). According to the results, it was found that paeonol could play the role of anti-atherosclerosis by up-regulating the expression of caveolin-1 and inhibiting the activation of NF-κB pathway to reduce vascular inflammation in atherosclerotic rats.

Aberrant oxidative metabolism in cells is one of the hallmarks of cancer. Overproduction of reactive species promotes carcinogenesis by inducing genetic mutations and activating oncogenic pathways, and thus, antioxidant therapy is considered as an important strategy for cancer prevention and treatment. Caveolin-1 (Cav-1), a constituent protein of caveolae, is involved in not only the formation of the caveolae, vesicular transport, maintaining cholesterol homeostasis directly, but also many cellular physiological and pathological processes including growth, regulation of mitochondrial antioxidant level, apoptosis and carcinomas by interacting with a lot of signaling molecules through caveolin scaffolding domain. Cav-1 has also been shown to mediate tumor genesis and progression through oxidative stress modulation, while Cav-1-targeted treatment could scavenge the reactive species. Intracellular reactive species could modulate the expression, degradation, post-translational modifications and membrane trafficking of Cav-1. More importantly, emerging evidence has indicated that multiple antioxidants could exert antitumor activities in cancer cells by modulating the signaling of Cav-1. This paper reviewed the research progresses on the roles of Cav-1 and oxidative stress in tumorigenesis and development, and would provide new insights on designing strategies for cancer prevention or treatment.

Objective: To investigate the effect and mechanism of hydroxyfasudi (HF), a specific Rho kinase inhibitor, on lipopolysaccharide(LPS)induced endothelial dysfunction. Methods: A total of 24 male Sprague Dawley rats were randomly divided into control group( n =6), HF group( n =6), LPS group( n =6) and LPS + HF group( n =6) with random number table method. There was no special treatment in control group. HF (30 mg/kg) was injected intraperitoneally in HF group. LPS (1 mg/kg) were injected intravenously in LPS group. In LPS+ HF group, HF (30 mg/kg) was injected intraperitoneally, followed by intravenous LPS injection (1 mg/kg) 30 minutes later. All rats were sacrificed after 8 hours, and aortic tissue was extracted. RT-PCR was performed to detect mRNA levels of Rho-associated coiled-coil protein kinase (ROCK)1, connexin (Cx)43 and caveolin (Cav)1. The protein levers of ROCK1, Cx43 and Cav-1 were assessed by Western blot and immunohistochemical staining respectively. Results: (1) RT-PCR experiments showed that mRNA levels of ROCK1(2.67±0.03 vs. 1.00±0.04), Cx43(1.73±0.03 vs. 1.00±0.08), and Cav1(1.85±0.04 vs. 1.0±0.03) in LPS group were significantly higher than in control group(all P <0.05). mRNA levels of ROCK1(0.38±0.02), Cx43(0.58±0.02), and Cav1(0.27±0.01) in LPS + HF group were significantly lower than in LPS group(all P <0.05). (2)Western blot analysis showed that protein levels of ROCK1(3.46±0.82 vs. 2.19±0.56), Cx43(0.33±0.09 vs.0.11±0.06), and Cav1(3.45±0.74 vs. 2.25±0.91) in LPS group were significantly higher than in control group(all P <0.05). Protein levels of ROCK1(1.09±0.52), Cx43(0.01±0.06), and Cav1(2.06±0.40) in LPS + HF group were significantly lower than in LPS group(all P <0.05). (3) Immunohistochemical staining showed that protein levels of ROCK1(84.1±0.953.7±2.9), Cx43(99.1±2.1 vs. 46.2±0.8), and Cav1(167.0±6.4 vs. 84.9±1.0) in LPS group were significantly higher than in control group(all P <0.05). Protein levels of ROCK1(30.4±0.6), Cx43(21.4±1.3), and Cav1(55.8±2.8) in LPS + HF group were significantly lower than in LPS group(all P <0.05). Conclusion: HF attenuates LPS induced endothelial dysfunction probably via suppressing the expression of ROCK1, Cx43 and Cav1.

Objective: To determine whether the inhibition of caveolin-1 tyrosine residues 14 (Cav-1-Y14) phosphorylation with protein tyrosine kinase inhibitors (PP2) will upregulate heme oxygenase-1 (HO-1) activity to protect against ventilation induced lung injury in vivo of an animal model., Methods: Fifty-four male Sprague-Dawley (SD) rats were randomly divided into nine groups (each n=6). Group A served as normal control group, in which rats did not receive ventilation but tracheotomy. Groups B1 and B2 received lung protective ventilation respectively for 1 hour or 2 hours. Groups C1 and C2 received high tidal volume (40 mL/kg) ventilation for 1 hour or 2 hours, respectively. The group D1 or D2 also received high tidal volume ventilation for 1 hour or 2 hour respectively, but they were given PP2 1 hour before high tidal volume ventilation. The groups E1 and E2 also received high tidal volume ventilation respectively for 1 hour or 2 hours, but tyrosine kinase inhibitor PP2 and HO-1 inhibitor zinc protoporphyrin IX (ZnPPIX) were given to animals 18 hours before high tidal volume ventilation. All the animals were sacrificed after ventilation, and the specimens of lung tissues and bronchoalveolar lavage fluid (BALF) were harvested. Then the changes in pathology of lung tissue was observed, and diffuse alveolar damage scores (DAD) were calculated, myeloperoxidase (MPO) activity was measured by colorimetric analysis, lung wet/dry ratio (W/D) was estimated. The expressions of phosphorylated caveolin-1 (P-Cav-1-Y14), caveolin-1 (Cav-1) and HO-1 were determined by Western Blot. The expressions of high mobility group B1 (HMGB1) and advanced glycation end product receptor (RAGE) in lung tissues were assayed with immunohistochemistry staining. The levels of tumor necrosis factor-α(TNF-α) in BALF were measured by enzyme linked immunosorbent assay (ELISA)., Results: There was no significant difference in all the parameters between group A and groups B. Compared with group B1, DAD score, W/D ratio, the activity of MPO and the concentration of TNF-α in BALF in group C1 were significantly increased [ DAD score: 7.97±0.59 vs. 0.55±0.13, W/D ratio: 5.70±1.61 vs. 5.04±0.63, MPO (U/g): 1.82±0.14 vs. 0.77±0.26, TNF-α (ng/L): 370.10±29.61 vs. 54.38±8.18, all P<0.05], and the injury in ventilation 2 hours group was more serious than that in ventilation 1 hour group. Compared with groups C, all the parameters in groups D were significantly decreased. The parameters in groups E were significantly higher than those in groups A, B, and D, but no significant difference was found as compared with groups C. Compared with groups B, the protein expressions of Cav-1 and P-Cav-1-Y14 (gray value) in groups C were significantly increased (1 hour: 1.49±0.02 vs. 1.26±0.13, 1.34±0.02 vs. 0.87±0.04; 2 hours: 1.58±0.02 vs. 1.27±0.27, 1.31±0.01 vs. 0.95±0.02, all P<0.05), and the expression of HO-1 protein (gray value) was significantly decreased (1 hour: 0.59±0.02 vs. 1.10±0.01, 2 hours: 0.49±0.01 vs. 1.20±0.02, both P<0.05). No significant difference in Cav-1 protein expression between groups D as well as groups E and groups C. The protein expression of P-Cav-1-Y14 in groups D and E was significantly lower than that in groups C. The protein expression of HO-1 in groups D was significantly higher than that in groups C, but the phenomenon was not found in groups E as compared with groups C. Compared with group A, the positive expression of HMGB1 and RAGE in lung tissue in groups C and E was significantly increased, but no significant difference was found between groups B as well as groups D and group A., Conclusions: Cav-1-Y14 phosphorylation is the key factor for ventilator induced lung injury, which can not only lead to a decrease in vascular barrier function, but also inhibit the activity of HO-1 enzyme, thus further aggravates inflammatory injury of the lung as induced by mechanical ventilation.

Objective: To explore the expression of caveolin-1 (Cav-1) induced by interleukin-17F/IL-17 receptor C (IL-17F/IL-17RC) in rat pulmonary microvascular endothelial cells (PMVECs)., Methods: Cultured PMVECs were divided into two groups of time-dependent experiment and IL-17RC signal pathway intervention according to the results of time-dependent experimental group: namely peak time of IL-17F-induced Cav-1 and its phosphorylation (p-Cav-1) expression of PMVEC for formulating the incubation time between IL-17F and PMVEC in IL-17RC signal pathway intervention group. Time-dependent experiment group: Western blot was used to detect the expression of Cav-1 after IL-17F stimulation for 0, 0.5, 1.5, 3.0, 6.0, 12.0, 24.0 h. Cav-1 and its phosphorylation expression after IL-17F challenge for 0, 10, 30, 60, 90, 120 min were evaluated by Western blot. IL-17RC signal pathway intervention group: PMVECs were divided into two groups after a 3-day pre-treatment of siRNA. The first group received a 60-min stimulation of 100 ng/ml IL-17F before detecting the expression of p-Cav-1 while the second group was subject to a 24-hour stimulation of 100 ng/ml IL-17F before detection. In addition, control, meaningless-siRNA, IL-17RC-siRNA, IL-17F and meaningless-siRNA + IL-17F groups were set as references for two groups respectively., Results: IL-17F up-regulated the expression of Cav-1 in a time-dependent manner. At 0, 0.5, 1.5, 3.0, 6.0, 12.0, 24.0 h, the relative expression levels of Cav-1 were (1.139 ± 0.134), (1.276 ± 0.166), (1.604 ± 0.080), (2.115 ± 0.231), (2.763 ± 0.226), (3.309 ± 0.493) and (3.963 ± 0.169). At 1.5 h, it was significantly higher than 0 h, peaked at 24.0 h and remained significantly higher than 0, 0.5, 1.5, 3.0, 6.0, 12.0 h (all P < 0.05). And IL-17F increased the expression of p-Cav-1 in a time-dependent manner. At 0, 10, 30, 60, 90, 120 min, the relative expression levels of p-Cav-1 were (0.540 ± 0.085), (0.880 ± 0.084), (1.437 ± 0.297), (1.491 ± 0.212), (1.017 ± 0.210) and (0.882 ± 0.074). At 10 min, p-Cav-1 was significantly higher than 0 min, peaked at 60 min, remained significantly higher than 0, 10, 30, 90, 120 min (all P < 0.05) and gradually decreased. At 120 min, it was still higher than 0 min. Compared with IL-17F group, IL-17RC-siRNA significantly inhibited IL-17F-induced Cav-1 and its phosphorylation (2.126 ± 0.318 vs 3.897 ± 0.424 and 1.014 ± 0.136 vs 1.431 ± 0.298, all P < 0.05)., Conclusions: IL-17F up-regulates the expressions of Cav-1 and p-Cav-1 in a time-dependent manner in PMVECs. And the silenced expression of IL-17RC in PMVECs by IL-17RC-siRNA significantly inhibits the IL-17F-induced expressions of Cav-1 and p-Cav-1.

Objective: To explore the expression and role of Caveolin-1 in the angiogenesis of cerebral arteriovenous malformation (AVM)., Methods: A total of 55 fresh AVM samples at Affiliated Hospital, Inner Mongolia Medical University and Beijing Tiantan Hospital from August 2013 to May 2014 were collected to test the expressions of Caveolin-1, vascular endothelial growth factor (VEGF), vascular endothelial growth factor-receptor 2 (VEGF-R2) and endothelial nitric oxide synthase (eNOS) by immunohistochemistry and Western blot. And the relationship between the expressions of Caveolin-1 and VEGF, VEGF-R2 and eNOS was analysed., Results: The expression rates of Caveolin-1, VEGF, VEGF-R2 and eNOS in human AVM were 100%, 87.27%, 76.36% and 85.45%. And the values were significantly higher than those in normal superficial temporal artery. Western blot showed that the expressions of Caveolin-1, VEGF, VEGF-R2 and eNOS in hemorrahge AVM were higher than those in non-hemorrahge counterpart (P < 0.05). The expressions of Caveolin-1, VEGF, VEGF-R2 and eNOS were consistent., Conclusion: Caveolin-1 plays a positive regulatory role in the angiogenesis of AVM through the PI3K/Akt signaling pathway. In cerebral AVM, Caveolin-1 plays an important role in occurrence, progression, hemorrahge and degradation of brain AVM.

For lack of the biomarker, early diagnosis of prostate cancer is often difficult. Caveolin-1 (Cav-1) is an important oncogene and a major structural coat protein of caveolae, which is involved in multiple cellular functions including molecular transport, cell adhesion, and signal transduction, as well as in the development and progression of prostate cancer. Cav-1 is secreted as a biologically active molecule that promotes cell survival and angiogenesis within the tumor microenvironment, and is overexpressed in the metastatic and primary sites of human prostate cancer. Secreted Cav-1 can be detected in the peripheral blood, and its expression level has an indicative value in the diagnosis and prognosis of prostate cancer. This review focuses on the structure and biological characteristics of Cav-1 and its correlation with prostate cancer.

Objective: To observe the distribution and expression changes of caveolin-1 under shear stress in a turbulence flow channel model mimicking susceptible sites of atherosclerosis in vitro., Methods: Human umbilical vein endothelial cells (HUVECs) were inoculated to flow channel and then exposed to disturbed shear stress for 6, 12, 24 and 48 hours, respectively. HUVECs inoculated to flow channel without shear stress served as controls. Immunofluorescence staining was performed with SABC-FITC to detect the caveolin-1 distribution and RT-PCR was used to determine the mRNA expression of caveolin-1 gene in these cells., Results: Confocal microcopy revealed ellipse-like shaped HUVECs under disturbed shear stress and caveolin-1 didn't move toward to the upstream edge of HUVECs but moved toward to the edge of HUVECs, and expression of caveolin-1 gene in HUVECs was significantly downregulated after exposure to shear stress for 48 hours compared to HUVECs without shear stress stimulation., Conclusion: Disturbed shear stress affected disposition and expression of caveolin-1 which might be responsible for shear stress induced endothelial cell pathological atherosclerotic changes.

To study the influence of hypercholesterolemia with caveolin-1 on the plasmalemma of vascular endothelium, we used the methods of immunohistochemistry to detect the dynamic changes of caveolin-1 in cultured ECV-304 cells which were stimulated high cholesterol serum and the arterial endothelium of hypercholesterolemia rats. It is resulted that high cholesteorol level can upregulate the expression of caveolin-1 both in vitro and in vivo. In the initial stage of hypercholesterolemia model, the expression of caveolin-1 increased as the time of high cholesterol level added, but in the later period it was decreased slightly.