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1.
Anatomy & Cell Biology ; : 150-157, 2018.
Article in English | WPRIM | ID: wpr-717228

ABSTRACT

In and after the third trimester, the lung surface is likely to become smooth to facilitate respiratory movements. However, there are no detailed descriptions as to when and how the lung surface becomes regular. According to our observations of 33 fetuses at 9–16 weeks of gestation (crown-rump length [CRL], 39–125 mm), the lung surface, especially its lateral (costal) surface, was comparatively rough due to rapid branching and outward growing of bronchioli at the pseudoglandular phase of lung development. The pulmonary pleura was thin and, beneath the surface mesothelium, no or little mesenchymal tissue was detectable. Veins and lymphatic vessels reached the lung surface until 9 weeks and 16 weeks, respectively. In contrast, in 8 fetuses at 26–34 weeks of gestation (CRL, 210–290 mm), the lung surface was almost smooth because, instead of bronchioli, the developing alveoli faced the external surfaces of the lung. Moreover, the submesothelial tissue became thick due to large numbers of dilated veins connected to deep intersegmental veins. CD34-positive, multilayered fibrous tissue was also evident beneath the mesothelium in these stages. The submesothelial tissue was much thicker at the basal and mediastinal surfaces compared to apical and costal surfaces. Overall, rather than by a mechanical stress from the thoracic wall and diaphragm, a smooth lung surface seemed to be established largely by the thick submesothelial tissue including veins and lymphatic vessels until 26 weeks.


Subject(s)
Female , Humans , Pregnancy , Diaphragm , Epithelium , Fetus , Lung , Lymphatic Vessels , Pleura , Pregnancy Trimester, Third , Stress, Mechanical , Thoracic Wall , Veins
2.
Chinese Journal of Nephrology ; (12): 553-557, 2012.
Article in Chinese | WPRIM | ID: wpr-429135

ABSTRACT

ObjectiveToexploretheeffectof ceremideonprocess of peritoneal mesothelial cells(PMCs) apoptosis induced by peritoneal dialysis solution(PDS).Methods PMCs were cultured with normal DMEM,1.5% PDS and 4.25% PDS.4.25% mannitol was used as high osmotic pressure control.Ceremide were detected by LC-MS-MS.Flow cytometry was used in apoptosis analysis.Bax,p53 and bcl-2 protein expressions were detected by Western blotting.Results (1) PDS caused the increase of intracellular ceremide in PMCs,and normal and high osmotic pressure controls had no such effect.As the acidic sphigomyelinase inhibitor,desipramine significantly inhibited the production of ceramide induced by 4.25% PDS [(56.08±12.24) μg/L vs (91.25:t:15.89) μg/L,P<0.01]. (2) Compared with 1.5% PDS,4.25% PDS stimulated PMCs apoptosis (26.65%±6.21% vs 4.04%±1.86%,P<0.01),up-regulated bax and p53 proteins expression (P<0.01),and down-regulated bcl-2 protein exprssion(P<0.05).Desipramine obviously inhibited the apoptosis induced by 4.25% PDS,decreased bax and p53 proteins expression,increased bcl-2 protein expression(P<0.05).Exogenous C2-ceremide reversed the effect of desipramine(P<0.05).Conclusion The increase of intracellular ceremide may play an important role in the PMCs apoptosis induced by high glucose PDS.

3.
Tuberculosis and Respiratory Diseases ; : 405-415, 2011.
Article in Korean | WPRIM | ID: wpr-181454

ABSTRACT

BACKGROUND: In an effort to find alternative therapeutic agents to prevent excessive fibrosis as a sequela to complicated parapneumonic effusion or empyema, we examined the effect of tissue plasminogen activator (tPA) as a fibrinolytic agent combined with talc or transforming growth factor (TGF)-beta1 in a human pleural mesothelial cell line, MeT-5A. METHODS: MeT-5A cells were stimulated with various doses of talc, doxycycline or TGF-beta1 for 24 h and then were treated with tPA for an additional 24 h. Cell viability was measured by MTT assay. The production of interleukin (IL)-8 and vascular endothelial growth factor (VEGF) in the culture supernatants was measured by ELISA. Real-time PCR was carried out for measurement of type I collagen mRNA. RESULTS: MeT-5A cells treated with talc showed a dose-dependent increase in production of IL-8. Talc also increased production of type I collagen mRNA at low doses, but talc did not influence the induction of VEGF. Addition of tPA to talc-stimulated cells showed further increases in the production of IL-8, but tPA did not influence the production of VEGF or type I collagen mRNA. TGF-beta1 increased the production of both VEGF and collagen type I mRNA, both of which were effectively inhibited by additional tPA treatment in MeT-5A cells. CONCLUSION: TGF-beta1 is a potent inducer of collagen synthesis without induction of IL-8 in MeT-5A cells. Addition of tPA after TGF-beta1 stimulation inhibited further fibrosis by direct inhibition of collagen mRNA synthesis as well as by inhibition of VEGF production.


Subject(s)
Humans , Cell Line , Cell Survival , Collagen , Collagen Type I , Doxycycline , Empyema , Enzyme-Linked Immunosorbent Assay , Epithelium , Fibrosis , Interleukin-8 , Interleukins , Real-Time Polymerase Chain Reaction , RNA, Messenger , Talc , Tissue Plasminogen Activator , Transforming Growth Factor beta1 , Transforming Growth Factors , Vascular Endothelial Growth Factor A
4.
Korean Journal of Pathology ; : 46-49, 2004.
Article in English | WPRIM | ID: wpr-118540

ABSTRACT

The presence of benign mesothelial cell inclusions in the mediastinal lymph node is extremely rare and thus difficult for the pathologist distinguishing from sinus histiocytosis, metastatic carcinoma, or metastatic mesothelioma. We recently had a case of benign mesothelial cell inclusions in the mediastinal lymph node, which is initially misinterpreted as metastatic carcinoma of unknown origin. However, further clinical studies failed to identify the primary site. Subsequent immunostaining with calretinin demonstrated the strong nuclear and cytoplasmic immunore-activity, suggesting that these cells are mesothelial cells. It is important that when the nodal changes resemble metastatic carcinoma morphologically in the mediastinal lymph nodes, but the primary site can not be identified clinically, the possibility of mesothelial cell inclusions should be raised and the proper use of immunohistochemistry in conjunction with a clinical finding is recommended.


Subject(s)
Calbindin 2 , Cytoplasm , Epithelium , Histiocytosis, Sinus , Immunohistochemistry , Lymph Nodes , Mediastinum , Mesothelioma
5.
Chinese Journal of Nephrology ; (12)1997.
Article in Chinese | WPRIM | ID: wpr-553957

ABSTRACT

Objective To study the gene and protein expression of matrix metalloproteinase 2 (MMP2) and its inhibitors TIMP1 and TIMP2 in human peritoneal mesothelial cells (HPMC), and the possible role of high glucose in submesothelial extracellular matrix (ECM) degradation during peritoneal dialysis (PD) . Methods Primary HPMC was isolated from spent peritoneal dialysis effluent collected from PD patients. After HPMC confluence, the cells were detached by trypsinization and passaged into 25 cm2 tissue-culture flasks. The effect of high glucose and hyperosmolarity on the gene expression of MMP2, TIMP1 and TIMP2 in HPMC was studied by semi-quantitative RT-PCR. Immunohistochemistry and zymography were used to measure the protein expression of MMP/TIMP in HPMC. Results HPMC expressed MMP2, TIMP1, TIMP2 at both gene and protein levels. 4. 25% glucose significantly up-regulated TIMP1 gene expression in HPMC( P

6.
Chinese Journal of Nephrology ; (12)1997.
Article in Chinese | WPRIM | ID: wpr-678357

ABSTRACT

Objective To investigate the mechanism of high-glucose-induced injury to human peritoneal mesothelial cells(HPMC). Methods (1)The cultured HPMCs were exposed to culture medium containing different concentrations of glucose(1. 5% , 2. 5% , 4. 25% )for 48 hours and 4. 25% mannitol and normal culture medium were as control. Then apoptosis was observed by flow cytometry and caspase-3 activity was measured by ApoAlert?CPP33/Caspase-3 Assay kits. (2) The cultured HPMCs were exposed to 4.25% glucose culture medium containing different concentrations of caspases inhibitor, Z-VAD. fmk (25, 50, 100 ?mol/L) for 48 hours and 4. 25% glucose culture medium containing DMSO was as control. Then apoptosis was observed by flow cytometry and caspase-3 activity was measured by ApoAlert?CPP33/ Caspase-3 Assay kits as well. Results (1) Glucose increased caspase-3 activity in a concentration-dependent manner. Compared to control, caspase-3 activity was significantly higher in 4. 25% glucose group and 2. 5% glucose group, but not significantly different in 1. 5% glucose group and 4. 25% mannitol group. (2) Apoptotic rate of HPMC was significantly lower in Z-VAD. fmk group than that in control. Z-VAD. fmk decreased the number of apoptotic cells in a concentration-dependent manner. Also, caspase-3 activity of HPMC was significantly lower in Z-VAD. fmk group than that in control. Conclutions (1) High-glucose can induce apoptosis and caspase-3 activation of HPMC in a dose-dependent manner. (2) Z-VAD. fmk inhibits high glucose-induced apoptosis of HPMC in a dose-dependent manner. (3)High glucose induces apoptosis of human peritoneal mesothelial cells by caspase-3 activation.

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