Atrial Fibrillation ; metabolism ; Connexin 43 ; metabolism ; Humans ; Oxidative Stress

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

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 examine the effect of acute incisional pain on the expression of connexin 43 in rat spinal cord dorsal horn.

METHODSEighty rats were assigned into control group without any treatment and incisional pain group with incision surgery. For paw incisions, a 1-cm longitudinal incision was made through the skin and fascia of the plantar aspect of the right hind paw. After surgery, the 50% paw withdrawal threshold (PWT) was assessed in response to a tactile stimulus with calibrated von Frey monofilaments at 1, 2, 4 and 24 h, respectively. The spinal cord dorsal horn of rats was isolated at 1, 2, and 4 h after the surgery to assess the expression of connexin 43 using Western blotting and immunofluorescence assay.

RESULTSThe 50% PWT of the rats was significantly decreased after the incision surgery, and this decrement was the most obvious at 2 and 4 h. Western blotting and immunofluorescence assay showed that the expression of connexin 43 in the spinal cord dorsal horn was significantly increased in rats receiving the surgery especially at 2 and 4 h after the surgery.

CONCLUSIONIncision surgery induces an significant increase in connexin 43 expression in rat spinal cord dorsal horn, suggestting an potential role of connexin43 in postoperative incisional pain.

Animals ; Connexin 43 ; metabolism ; Pain, Postoperative ; metabolism ; Rats ; Rats, Sprague-Dawley ; Spinal Cord Dorsal Horn ; metabolism

Gap junctions (GJ), as a special membrane structure between adjacent cells, are composed of connexins (Cx) and regulate the proliferation and differentiation of cells. Studies show that gap junctional intercellular communication is weakened or lost in most tumor cells and this abnormality is often accompanied by changed expression of Cxs. Cx43 is a major connexin in the testis tissue. This review focuses on the latest progress in the studies of Cx43 in testicular tumors.
Animals ; Cell Communication ; Cell Differentiation ; Connexin 43 ; metabolism ; Gap Junctions ; metabolism ; Male ; Testicular Neoplasms ; metabolism

OBJECTIVETo study the effect of gossypol on the expression of connexin 43 (CX43) in Sertoli cells.

METHODSTM4 Sertoli cells were cultured and treated with gossypol at the concentrations of 1.25, 2.5, 5 and 10 micromol/L for 6, 12, 24 and 48 hours. The cytotoxicity of gossypol was assessed by CCK-8 assay, and the expression of CX43 in the normal TM4 Sertoli cells and in those treated with different concentrations of gossypol for different times was detected by RT-PCR and immunofluorescence analysis.

RESULTSSemiquantitative RT-PCR and immunofluorescence analysis showed the expression of CX43 in the normal TM4 cells. At 24 hours of exposure to gossypol, the expression began to decrease gradually with the prolonging of time and the increasing concentration of gossypol (P < 0.05).

CONCLUSIONGossypol reduces the expression of CX43 in TM4 Sertoli cells, which might underlie the mechanism of its antifertility action.

Cells, Cultured ; Connexin 43 ; metabolism ; Gossypol ; toxicity ; Humans ; Male ; Sertoli Cells ; drug effects ; metabolism

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

OBJECTIVETo investigate the roles of mitochondrial connexin43 (Cx43) and mitochondrial ATP sensitive potassium channe1 (mitoK(ATP)+) in the postconditioning protection for rabbits underwent myocardial ischemia/reperfusion injury.

METHODSIn anesthetized open-chest rabbits, the left anterior descending artery (LAD) was occluded for 30 min and reperfused for 4 h and randomly divided into four groups (n = 16 each): sham operation group (Sham), ischemic reperfusion group (IR), ischemic postconditioning group (PC) and PC plus 5-HD, a specific mitoK(ATP)+ inhibitor (PC + 5-HD). Rabbits were sacrificed post 4 h reperfusion. Heart rate and the mean arterial pressure were recorded and plasma CK-MB and cTnI activity were measured at baseline, at the end of ischemia, and after 2 h and 4 h of reperfusion, respectively. Myocardial infarct size was determined and mitochondria structure was observed under electron microscope at the end of the experiment. Mitochondria were isolated and the protein content of the mitochondrial Cx43 was determined by Western blot.

RESULTSPlasma CK-MB, cTnI activity and myocardial infarct size were significantly reduced in PC [(19.1 +/- 3.9)%] group compared to IR [(35.7 +/- 5.8)%] and PC + 5HD [(34.2 +/- 3.9)%] groups (all P < 0.01). Degree of mitochondria damage was significantly reduced in PC group compared to IR and PC + 5HD groups (all P < 0.01). The mitochondria Cx43 content was significantly decreased in IR group and PC + 5-HD group compared to sham group (all P < 0.05) and restored in PC group.

CONCLUSIONIschemic postconditioning protected the heart from I/R injury by improving mitochondrial ultrastructure and by attenuating I/R induced decrease of mitochondria Cx43 expression. The protective effects of postconditioning was partly mediated by activating mitoK(ATP)+ pathway.

Animals ; Connexin 43 ; metabolism ; Disease Models, Animal ; Mitochondria ; metabolism ; Myocardial Reperfusion Injury ; metabolism ; Potassium Channels ; metabolism ; Rabbits

Animals ; Cardiomyopathy, Dilated ; metabolism ; Connexin 43 ; metabolism ; Disease Models, Animal ; Hypericum ; Male ; Plant Extracts ; pharmacology ; Rats ; Rats, Wistar

OBJECTIVETo investigate the role of gap junction in ischemic preconditioning (IPC).

METHODSSprague-Dawley rats were subjected to a 30 min coronary artery occlusion followed by 4 h of reperfusion (I/R). Rats were divided into seven groups: I/R, IPC/R, IPC/R + 5-hydroxydecanoic acid (mitochondrial ATP sensitive potassium channel antagonist), I/R + diazoxide (mitochondrial ATP sensitive potassium channel agonist), I/R + 5-hydroxydecanoic acid + diazoxide, I/R + 18beta-glycyrrhetinic acid (gap junction blocker) and I/R + 18beta-glycyrrhetinic acid + 5-hydroxydecanoic acid. Hemodynamics and myocardial infarct size were measured and connexin43 phosphorylation and subcellular distribution were determined by quantitative immunoblotting and confocal immunofluorescence.

RESULTSInfarct size was reduced in IPC/R, I/R + diazoxide and I/R + 18beta-glycyrrhetinic acid group (13.34% +/- 7.87%, 11.02% +/- 2.24%, and 15.03% +/- 11.35%, respectively; P < 0.001 vs. I/R group: 45.81% +/- 7.91%). 5-hydroxydecanoic acid abolished the cardioprotective effects of IPC and diazoxide (46.57% +/- 5.36% and 47.36% +/- 3.17%; P > 0.05 vs. I/R) but not the effects of glycyrrhetinic acid (14.60% +/- 7.36%; P < 0.001 vs. I/R). Phosphorylation of connexin43 was significantly increased, dephosphorylation and connexin43 intracellular redistribution significantly decreased (Cx43 size in the cellular membrane 1.00% +/- 0.35% and 0.83% +/- 0.31%, P < 0.001 vs. I/R: 0.19% +/- 0.06%) by IPC and diazoxide and these effects could be abolished by 5-hydroxydecanoic acid.

CONCLUSIONIschemic preconditioning could reduce myocardial infarction size by activating mitochondrial ATP sensitive potassium channel and modulating connexin43 phosphorylation and internalization.

Animals ; Connexin 43 ; metabolism ; Gap Junctions ; physiology ; Ischemic Preconditioning, Myocardial ; Male ; Myocardial Infarction ; metabolism ; pathology ; Phosphorylation ; Rats ; Rats, Sprague-Dawley