Atrial Fibrillation ; etiology ; Connexin 43 ; analysis ; Connexins ; analysis ; Fluorescent Antibody Technique ; Gap Junctions ; physiology ; Humans

OBJECTIVETo probe into expression of connexin 43 (Cx43) in the meridians of the normal healthy rats and the relation among connexin, gap junction and meridian.

METHODSPowerVision two step immunohistochemical technique and ASIAS-2000 automatical image-scan analyzing system were used to detect Cx43 level and distribution in the Kidney and Bladder Meridians of the rat.

RESULTSCx43 expressed mainly in skin epithelia, fibroblasts and mast cells of the subcutaneous layer. And expression of Cx43 in the Kidney and Bladder Meridians was significantly more than that in the control lines (P < 0.01).

CONCLUSIONConnexins and gap junctions have close relation with the meridians, and the gap junctional intercellular communication may play an important role in the function of meridians.

Animals ; Cell Communication ; Connexin 43 ; metabolism ; Connexins ; Gap Junctions ; metabolism ; Meridians ; Rats

We studied the sex different nicotine effect on evoked population spike amplitudes (ePSA) and connexin (Cx) expression in the hippocampus CA1 area of gerbils. Acute doses of nicotine bitartrate (0.5 mg/kg: NT-0.5) slightly reduced ePSA in males but markedly augmented that in females. Acute NT (5.0 mg/kg) markedly increased the ePSA in all gerbils. Unlike acute NT-0.5, repeated NT-0.5 injection (twice a day for 7 days) significantly increased the ePSA in males and slightly affected the NT-0.5 effect in females. The Cx36 and Cx43 expression levels as well as Cx expressing neuronal populations were significantly increased by repeated NT-0.5 in in both male and female gerbils, and particularly, Cx43 expression was somewhat prominent in females. These results demonstrated a sex difference with respect to the nicotine effect on hippocampal bisynaptic excitability, irrelevant to connexin expression.
Animals ; Connexins ; Connexin 43 ; Female ; Gerbillinae* ; Hippocampus ; Male ; Neurons* ; Nicotine* ; Sex Characteristics*

Objective To study the effect of overwork stress response on the expression of connexin 43（Cx43） and connexin 45（Cx45） in cardiomyocytes and on cardiac function. Methods The experimental animals were divided into control group, overworked 1-month group and overworked 2-month group. A overworked rat model was established by forcing swimming of overworked group. The expressions of Cx43 and Cx45 in myocardial tissues of experimental animals were detected by Western blotting, while the corresponding myocardial tissues were stained with hematoxylin-eosin （HE） staining and Masson's staining, then histologically observed. Results Western blotting results showed that, compared with the control group, Cx43 expression in myocardial tissues of overworked rats decreased while Cx45 expression increased. HE staining and Masson's staining results showed that hypertrophy, rupture and interstitial fiber tissue hyperplasia were observed in myocardial fibers of overworked rats. Conclusion Overwork stress response may affect cardiac function as an independent factor and may even cause heart failure or arrhythmias and lead to death.
Animals ; Arrhythmias, Cardiac/metabolism* ; Connexin 43/metabolism* ; Connexins/metabolism* ; Heart Failure ; Myocardium ; Myocytes, Cardiac/metabolism* ; Rats

OBJECTIVETo investigate the expressions of Cx26, Cx32 and Cx43 in prostate cancer (PCa) and benign prostatic hyperplasia (BPH) and their roles in the development and progression of PCa in order to provide some novel evidence for the diagnosis and treatment of PCa.

METHODSWe determined the expressions of Cx26, Cx32 and Cx43 in the paraffin samples from 31 cases of PCa and 23 cases of BPH by SABC immunohistochemical staining, and analyzed the relationship of their expressions with the clinical and pathological parameters of PCa and BPH using the semiquantitative method.

RESULTSThe positive expressions of Cx26 in BPH and PCa were 82.6% and 74.2%, respectively (chi2 = 0.541, P > 0.05), those of Cx32 were 78.3% and 61.3% (chi2 = 1.763, P > 0.05), and those of Cx43 were 87.0% and 38.7% (chi2 = 12.730, P < 0.01). The staining intensities of Cx26 and Cx43 were negatively correlated with the malignant phenotype of PCa (rCx26 = -0.476, P < 0.01; rCx43 = -0.484, P < 0.01), but not the expression of Cx32 (r = -0.242, P > 0.05). The three Cxs exhibited no correlation with the age and serum PSA level of the patients (P > 0.05), nor among their expressions (P > 0.05).

CONCLUSIONCx26, Cx32 and Cx43 are expressed in different degrees in BPH and PCa tissues. Cx43 plays a role in the occurrence and progression of PCa, and may serve as a new marker of PCa besides PSA as well as a new target in the biotherapy of PCa. Cx26 may be partially involved in the progression of PCa, but its mechanisms need to be further studied.

Aged ; Aged, 80 and over ; Connexin 26 ; Connexin 43 ; metabolism ; Connexins ; metabolism ; Humans ; Male ; Prostate ; metabolism ; Prostatic Neoplasms ; metabolism

PURPOSE: Detrusor overactivity is frequently associated with bladder outlet obstruction, which may be related with increased electrical coupling. The effects of connexin 43(Cx43) and connexin 26(Cx26) mRNA expressions on the detrusor over activity were studied. MATERIALS AND METHODS: 36 male patients, with a bladder outlet obstruction due to benign prostatic hyperplasia(BPH), were subdivided into those with and without detrusor overactivity(DO) based on urodynamic studies: DO(+) and DO(-) group. All patients underwent a bladder biopsy during TUR-P. The symptoms, International Prostate Symptom Score (IPSS), prostate size, serum prostatic specific antigen(PSA) value and urodynamic parameters were compared between the two groups. The expressions of Cx43 and Cx26 mRNA in each group were analyzed by a reverse transcriptase polymerase chain reaction(RT-PCR). RESULTS: There were no differences in age, IPSS score, prostate volume, PSA and free Qmax between the DO(+) and DO(-) groups. The expressions of Cx43 and Cx26 mRNA in the DO(+) group were significantly increased compared with those in the DO(-) group. CONCLUSIONS: Our results show there is a change in the expressions of the Cx43 and Cx26 according to the bladder function, which may be related to detrusor overactivity in patients with a bladder outlet obstruction.
Biopsy ; Connexin 43 ; Connexins ; Humans ; Male* ; Prostate ; Prostatic Hyperplasia* ; RNA, Messenger ; RNA-Directed DNA Polymerase ; Urinary Bladder Neck Obstruction* ; Urinary Bladder* ; Urodynamics

PURPOSE: Clinically, bladder outlet obstruction (BOO) causes not only obstructive symptoms but also overactive bladder symptoms which partially result from the increase of electrical coupling in the bladder. This study was performed to determine the effect of angiotensin converting enzyme (ACE) inhibitor on connexin (Cx) expression in overactive bladder caused by BOO in a rat model. MATERIALS AND METHODS: Fifty Sprague-Dawley rats were used for this study and divided into control (10 rats) and experimental (40 rats) groups. Partial obstruction was induced in the experimental group which was divided into two subgroups of 20 rats each: one group administered with ACE inhibitor (ACE inhibitor treated group) and the other without administration (obstruction group). Cystometrograms (CMG) were performed 2 weeks after BOO. The bladders of each group were dissected out and underwent staining for Cx26 and Cx43. RESULTS: On CMG, there was a significant decrease in contraction interval of the obstructive group compared with the control group. The ACE inhibitor treated group showed an increase in contraction interval compared with the obstruction group but a decrease in contraction interval compared with the control group (p<0.05). On immunohistochemical staining, Cx26 was localized in the mucosa and Cx43 in the mucosa and muscle layer. The staining intensity of Cx26 and Cx43 was increased in the obstructive group compared with the control group, but decreased in the ACE inhibitor treated group compared with the obstruction group. CONCLUSIONS: ACE inhibitor decreased the expression of Cx and relieved the overactive bladder symptom. Therefore, ACE inhibitor could be used as alternative agent for the treatment of overactive bladder associated with BOO.
Angiotensin-Converting Enzyme Inhibitors ; Animals ; Connexin 43 ; Connexins ; Models, Animal ; Mucous Membrane ; Peptidyl-Dipeptidase A ; Rats* ; Rats, Sprague-Dawley ; Urinary Bladder Neck Obstruction* ; Urinary Bladder* ; Urinary Bladder, Overactive

The postmortem diagnosis of ischemic heart disease is sometimes difficult for forensic pathologists especially when microscopic ischemic change in the myocardium is not detected at the early stages of ischemic injury by conventional staining techniques. Connexin 43 (Cx43) is a gap junction protein in human myocardium, which is phosphorylated and localized to the intercalated discs in the normal cardiac muscles. However, during ischemia and hypoxia, total Cx43 (tCx43) undergoes progressive dephosphorylation and concomitant accumulation of non-phosphorylated Cx43 (npCx43) at the lateral cell borders. This study was aimed to evaluate the efficacy of the immunohistochemical expression of Cx43 in the myocardium as an early ischemic marker in forensic autopsy. The study group consisted of 24 cases listing patients who died of ischemic heart disease (IHD) with severe coronary atherosclerosis that showed no myocardial pathology. Cases of sudden death of individuals from non-IHD (n=16) were used as controls. The survival times in both IHD and non-IHD groups were within 24 hours of the onset of angina symptoms, related injury, or the event for the cause of death. There was a statistically significant difference in tCx43 and npCX43 immunopositivity in the IHD group due to their expression patterns. In the IHD group, the redistribution of Cx43 expression from the intercalated discs to the lateral cell borders occurred more frequently than in the non-IHD group. In conclusion, the different expression patterns of tCx43 and npCx43 in the myocardium in IHD could be used as adjunctive ischemic markers.
Anoxia ; Autopsy* ; Cause of Death ; Connexin 43* ; Connexins ; Coronary Artery Disease ; Death, Sudden ; Diagnosis ; Forensic Pathology ; Humans ; Immunohistochemistry ; Ischemia ; Myocardial Ischemia ; Myocardium* ; Pathology

PURPOSE: Connexins (Cx) constitute a family of transmembrane proteins that form gap junction channels, and allow metabolic and electrical coupling of cellular networks. This study was undertaken to evaluate the regulation of Cx expression, according to bladder function, after the relief of a bladder outlet obstruction in rat. MATERIALS AND METHODS: 50 Wistar male rats were used for this study. They were divided into two groups: 10 in a control group, and 40 in an experimental group. The experimental group was partially obstructed for 3 weeks, after which the obstruction was relieved by urethral deligation. 3 weeks after the deligation, cystometrograms (CMG) were performed. On the basis of the CMG results, the experimental group was subdivided into the normalized and unstable groups. The bladders from each group were dissected after the CMG, and weighed. The expressions of Cx43 and Cx40 mRNA in each group were analyzed by a reverse transcriptase polymerase chain reaction (RT-PCR). RESULTS: The bladder weights of both the normalized and unstable groups increased compared with the control group (p<0.05). On CMG, the contraction interval of the unstable group was markedly decreased compared with that of the control and normalized groups (p<0.05). The semiquantitative RT-PCR revealed that there was no significant difference in the expressions of Cx43 mRNA between the control and normalized groups. However, the expression of Cx43 mRNA of the unstable group was significantly increased compared with the control and normalized groups. The expression of Cx40 mRNA was no different between the groups. CONCLUSIONS: Our results show that there is a change in the expressions of the onnexins according to bladder function, which may be related to a persistent unstable bladder or irritative symptoms following the relief of a bladder outlet obstruction.
Animals ; Connexin 43 ; Connexins ; Gap Junctions ; Humans ; Male ; Rats* ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger ; Urinary Bladder Neck Obstruction* ; Urinary Bladder* ; Weights and Measures

Connexin 43 ; genetics ; Connexins ; genetics ; Heart Defects, Congenital ; genetics ; Homeobox Protein Nkx-2.5 ; Homeodomain Proteins ; genetics ; Humans ; Infant ; Infant, Newborn ; Mutation ; genetics ; Myocardium ; metabolism ; Transcription Factors ; genetics