Cardiovascular System ; pathology ; China ; Humans

Lipoma preferred partner (LPP) has been identified as a protein which is highly selective for smooth muscle progenitor cells (SMPCs) and regulates differentiation and migration of SMPCs, but mechanisms of LPP expression are not elucidated clearly. The aim of the present study was to discuss the mechanisms by which LPP expression is regulated in the differentiation and migration of SMPCs induced by TGF-β1. It was found that TGF-β1 could significantly increase the expression of LPP, smooth muscle α-actin, smooth muscle myosin heavy chain (SM-MHC), and smoothelin in SMPCs. Moreover, inactivation of Rho kinase (ROK) with ROK inhibitors significantly inhibited LPP mRNA expression in TGF-β1-treated SMPCs and mouse aortic smooth muscle cells (MAoSMCs). At the same time, LPP silencing with short interfering RNA significantly decreased SMPCs migration. In conclusion, LPP appears to be a ROK-dependant SMPCs differentiation marker that plays a role in regulating SMPCs migration.
Animals ; Bone Marrow ; metabolism ; physiology ; Cell Differentiation ; genetics ; Cell Movement ; genetics ; Cells, Cultured ; Cytoskeletal Proteins ; genetics ; metabolism ; LIM Domain Proteins ; genetics ; metabolism ; Mice ; Mice, Inbred C57BL ; Muscle, Smooth ; metabolism ; physiology ; Stem Cells ; metabolism ; physiology ; Transforming Growth Factor beta1 ; genetics ; metabolism ; rho-Associated Kinases ; genetics ; metabolism

Lipoma preferred partner (LPP) has been identified as a protein which is highly selective for smooth muscle progenitor cells (SMPCs) and regulates differentiation and migration of SMPCs, but mechanisms of LPP expression are not elucidated clearly. The aim of the present study was to discuss the mechanisms by which LPP expression is regulated in the differentiation and migration of SMPCs induced by TGF-β1. It was found that TGF-β1 could significantly increase the expression of LPP, smooth muscle α-actin, smooth muscle myosin heavy chain (SM-MHC), and smoothelin in SMPCs. Moreover, inactivation of Rho kinase (ROK) with ROK inhibitors significantly inhibited LPP mRNA expression in TGF-β1-treated SMPCs and mouse aortic smooth muscle cells (MAoSMCs). At the same time, LPP silencing with short interfering RNA significantly decreased SMPCs migration. In conclusion, LPP appears to be a ROK-dependant SMPCs differentiation marker that plays a role in regulating SMPCs migration.

In order to explore the value of p63, smoothmuscle actin (alpha-SMA) and cytokeratin 5/6 (CK5/6) in the differential diagnosis of ductal lesions of breast, 88 tissue specimens of ductal lesions of breast were collected and examined histologically by HE staining. By using immunohistochemistry, the expression of p63, alpha-SMA and CK5/6 was detected. The results showed that in 38 cases of benign breast lesions, the proliferating cells were all positive for p63 and alpha-SMA. In 19 cases of ductal carcinoma in situ (DCIS) and 7 cases of intraductal papillary carcinoma, alpha-SMA positive cells formed a layer of continuous embroider-shaped structure and the p63 positive cells formed a layer of evenly separated embroider-shaped structure around the ducts. There was no cross-reaction between p63 and interstitial myofibroblasts and vascular smooth muscle cells. In 38 cases of benign breast lesions, the positive rate of CK5/6 expression was 100%. In 5 cases of atypical ductal hyperplasia, there were few positive cells in the ducts. In 19 cases of CDIS, no tumor cells expressed CK5/6. In 19 cases of invasive ductal carcinoma, almost no CK5/6 was detectable. It was suggested that p63 could serve as a novel specific marker for the identification of breast myoepithelial cells. CK5/6 is of value in differentiating ductal proliferation of varying degrees, especially in the differentiation between cancerous and non-cancerous changes. Simultaneous detection of p63, CK5/6 and alpha-SMA can help increase the diagnostic accuracy of breast diseases.

In order to explore the value of p63, smooth muscle actin (α-SMA) and cytokeratin 5/6(CK5/6) in the differential diagnosis of ductal lesions of breast, 88 tissue specimens of ductal lesions of breast were collected and examined histologically by HE staining. By using immunohistochemistry,the expression of p63, α-SMA and CK5/6 was detected. The results showed that in 38 cases of benign breast lesions, the proliferating cells were all positive for p63 and α-SMA. In 19 cases of ductal carcinoma in situ (DCIS) and 7 cases of intraductal papillary carcinoma, α-SMA positive cells formed a layer of continuous embroider-shaped structure and the p63 positive cells formed a layer of evenly separated embroider-shaped structure around the ducts. There was no cross-reaction between p63 and interstitial myofibroblasts and vascular smooth muscle cells. In 38 cases of benign breast lesions, the positive rate of CK5/6 expression was 100 %. In 5 cases of atypical ductal hyperplasia, there were few positive cells in the ducts. In 19 cases of CDIS, no tumor cells expressed CK5/6. In 19 cases of invasive ductal carcinoma, almost no CK5/6 was detectable. It was suggested that p63 could serve as a novel specific marker for the identification of breast myoepithelial cells. CK5/6 is of value in differentiating ductal proliferation of varying degrees, especially in the differentiation between cancerous and non-cancerous changes. Simultaneous detection of p63, CK5/6 and α-SMA can help increase the diagnostic accuracy of breast diseases.

To investigate the immunophenotypings of malignant epithelial mesothelioma (MEM), and to seek the valuable markers in distinguishing peritoneal MEM from peritoneal metastatic ovarian adenocarcinoma (OA) and colorectal adenocarcinoma (CA), immunohistochemical SP method was used to detect expressions of HBME-1, E-cadherin, CA19-9, MOC-31 and CK7 in paraffin-embedded tissues of 18 cases of MEM, 20 OA and 20 CA. The results showed that there was a significant difference in the expressions of E-cadherin, CA19-9 and MOC-31 between MEM and OA group (P<0.05). Similarly, the difference in the expression of HBME-1, E-cadherin, CA19-9, MOC-31 and CK7 between MEM and CA groups is significant (P<0.05). These results indicate that HBME-1 could be used as a positive marker in distinguishing MEM from CA. E-cadherin, CA19-9 and MOC-31 are considered to be useful negative markers in diagnostic distinction between MEM and metastatic adenocarcinomas, including OA and CA. CK7 is the best positive marker in distinguishing MEM from CA, but this marker appears to be valueless in discriminating MEM from OA.
Adenocarcinoma ; diagnosis ; pathology ; Colorectal Neoplasms ; complications ; diagnosis ; pathology ; Cystadenocarcinoma, Mucinous ; diagnosis ; pathology ; Cystadenocarcinoma, Serous ; diagnosis ; pathology ; Diagnosis, Differential ; Female ; Humans ; Immunophenotyping ; Male ; Mesothelioma ; diagnosis ; etiology ; pathology ; Ovarian Neoplasms ; complications ; diagnosis ; pathology ; Peritoneal Neoplasms ; diagnosis ; etiology ; pathology

To investigate the immunophenotypings of malignant epithelial mesothelioma (MEM), and to seek the valuable markers in distinguishing peritoneal MEM from peritoneal metastatic ovarian adenocarcinoma (OA) and colorectal adenocarcinoma (CA), immunohistochemical SP method was used to detect expressions of HBME-1, E-cadherin, CA19-9, MOC-31 and CK7 in paraffin-embedded tissues of 18 cases of MEM, 20 OA and 20 CA. The results showed that there was a significant difference in the expressions of E-cadherin, CA19-9 and MOC-31 between MEM and OA group (P<0.05). Similarly, the difference in the expression of HBME-1, E-cadherin, CA19-9, MOC-31 and CK7 between MEM and CA groups is significant (P<0.05). These results indicate that HBME-1 could be used as a positive marker in distinguishing MEM from CA. E-cadherin, CA19-9 and MOC-31 are considered to be useful negative markers in diagnostic distinction between MEM and metastatic adenocarcinomas, including OA and CA. CK7 is the best positive marker in distinguishing MEM from CA, but this marker appears to be valueless in discriminating MEM from OA.

To study the resistant mechanism and clinical significance of pseudomonas aeruginosa to beta-lactam antibiotics, the outer membrane permeability rate of 30 P. aeruginosa strains to 5 beta-lactam antibiotics was measured and their production of beta-lactamase and the beta-lactamase genes they carried detected. Furthermore, the relationship between the permeability, beta-lactamase and the clinical effects of beta-lactam antibiotics was observed. By using 14C-penicillin and liquid-scintillant isotope assay, the affinity of penicillin binding proteins (PBPS) was measured and their roles in the resistant mechanism studied. It was revealed that the permeability rate was higher in sensitive strains than in resistant ones (P < 0.05). All strains harbored 1-4 beta-lactamase genes and produced beta-lactamase. Higher permeability rate and higher degree of stability to beta-lactamase indicated better clinical therapeutic effects. The affinity of PBPs changed little without regard to the permeability and beta-lactamase. These results suggested that the permeability of outer membrane and beta-lactamase, but not PBPs, played important roles in the resistant mechanism of P. aeruginosa to beta-lactam antibiotics and affected the clinical therapeutic effectiveness of some patients.
Anti-Bacterial Agents ; pharmacology ; Bacterial Outer Membrane Proteins ; metabolism ; Humans ; Microbial Sensitivity Tests ; Permeability ; Pseudomonas aeruginosa ; drug effects ; beta-Lactam Resistance ; genetics ; beta-Lactamases ; metabolism ; beta-Lactams ; pharmacology

By study on the effect of anisodamine on lipopolysaccharide-induced expression of tissue factor (TF) in vascular endothelial cells (EC), the mechanism of anisodamine antithrombosis, as well as in the treatment of bacteraemic shock was investigated. Human umbilical vein endothelial cells (HUVECs) were cultured by trypsin digestion method. TF activity was measured in the lysates of HUVEC by using a single step clotting assay. Specific mRNA expression was detected by Northern blotting. In order to evaluate a possible contribution of the nuclear factor (NF)-kappa B pathway on the effects observed, electrophoretic mobility shift assays (EMSA) were performed using nuclear extracts from HUVECs and NF-kappa B-binding oligonucleotides. The results showed that treatment of HUVEC with LPS resulted in a significant increase in TF activity. Anisodamine dose-dependently inhibited LPS-induced upregulation of TF. These effects was also confirmed on the level of specific TF mRNA expression by Northern blotting. Furthermore, EMSA showed that anisodamine completely abolished LPS-induced NF-kappa B DNA binding activity in nuclear extracts from HUVECs treated with LPS together with anisodamine. The results suggest that anisodamine counteracts endothelial cell activation by inhibiting LPS-induced TF expression in these cells. Its interference with the NF-kappa B pathway might--at least in part--contribute to this effect. The ability of anisodamine to counteract LPS effect on endothelial cells might be one underlying mechanism explaining its antithrombosis and efficacy in the treatment of bacteraemic shock.
Cells, Cultured ; Drugs, Chinese Herbal ; pharmacology ; Electrophoretic Mobility Shift Assay ; Endothelium, Vascular ; metabolism ; Humans ; Lipopolysaccharides ; NF-kappa B ; biosynthesis ; genetics ; RNA, Messenger ; biosynthesis ; genetics ; Solanaceous Alkaloids ; pharmacology ; Thromboplastin ; biosynthesis ; genetics ; Umbilical Veins ; cytology

To study the resistant mechanism and clinical significance of pseudomonas aeruginosa to beta-lactam antibiotics, the outer membrane permeability rate of 30 P. aeruginosa strains to 5 beta-lactam antibiotics was measured and their production of beta-lactamase and the beta-lactamase genes they carried detected. Furthermore, the relationship between the permeability, beta-lactamase and the clinical effects of beta-lactam antibiotics was observed. By using 14C-penicillin and liquid-scintillant isotope assay, the affinity of penicillin binding proteins (PBPS) was measured and their roles in the resistant mechanism studied. It was revealed that the permeability rate was higher in sensitive strains than in resistant ones (P < 0.05). All strains harbored 1-4 beta-lactamase genes and produced beta-lactamase. Higher permeability rate and higher degree of stability to beta-lactamase indicated better clinical therapeutic effects. The affinity of PBPs changed little without regard to the permeability and beta-lactamase. These results suggested that the permeability of outer membrane and beta-lactamase, but not PBPs, played important roles in the resistant mechanism of P. aeruginosa to beta-lactam antibiotics and affected the clinical therapeutic effectiveness of some patients.
Anti-Bacterial Agents/*pharmacology ; Bacterial Outer Membrane Proteins/metabolism ; Microbial Sensitivity Tests ; Permeability ; Pseudomonas aeruginosa/*drug effects ; beta-Lactam Resistance/*genetics ; beta-Lactamases/metabolism ; beta-Lactams/*pharmacology