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Anticancer Res. 2002 Nov-Dec;22(6A):3383-8.
Expression of cathepsin D in urothelial carcinoma of the urinary bladder: an immunohistochemical study including correlations with extracellular matrix components, CD44, p53, Rb, c-erbB-2 and the proliferation indices.
Ioachim E, Charchanti A, Stavropoulos N, Athanassiou E, Bafa M, Agnantis NJ.
Department of Pathology, Medical School, University of Ioannina, 45110 Ioannina, Greece. ioachimtenet.gr
The immunohistochemical Cathepsin D (CD) expression of tumor and stromal cells was investigated in a series of 77 urothelial carcinomas of the urinary bladder with the intention to evaluate its prognostic significance and its contribution to the metastatic potential of bladder cancer. CD expression (clone D13A) was correlated with the expression of extracellular matrix components (collagen type IV, laminin, fibronectin), CD44, p53, pRb, proliferation indices (PCNA and MIB1) as well as with other conventional clininopathological features. CD expression (> 10% of positive tumor cells) was observed in 77.9% of the carcinomas. Stromal CD expression was detected in all cases. Linear collagen type IV and laminin deposit at the tumor-stroma border (in > 25% of the BM) was found in 26% and 57.6% of the cases, respectively. The CD of cancer cells (CCCD) was inversely-correlated with the CD of the stromal cells (p = 0.039), tumor grade (p = 0.0028), tumor stage (p = 0.0046), p53 protein (p = 0.05) and positively-correlated with CD44 (p = 0.002) and pRb (p = 0.05). The stromal cells CD (SCCD) showed a statistically significant positive correlation with tumor grade (p < 0.0001) and stage (p = 0.0001), and the proliferation indices PCNA and MIB1 (p = 0.0001 and p = 0.0002, respectively). These data suggest that both CD of tumor and stromal cells could play important roles in the expansion of urothelial carcinoma of the urinary bladder.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12530091&dopt=Abstract
J Invest Dermatol. 2003 Jan;120(1):116-22.
IL-12 completely blocks ultraviolet-induced secretion of tumor necrosis factor alpha from cultured skin fibroblasts and keratinocytes.
Werth VP, Bashir MM, Zhang W.
Department of Dermatology, University of Pennsylvania and Philadelphia V.A. Hospital, Philadelphia, Pennsylvania 19104, USA. wertail.med.upenn.edu
Interleukin-12 is an important regulator of other cytokines. Although interleukin-12 is considered to act primarily on lymphocytes, provoking a shift from T helper 2 to T helper 1 cells and an increase in lymphocyte-derived tumor necrosis factor alpha, we hypothesized that interleukin-12 might also affect tumor necrosis factor alpha secretion from skin cells. In this study, keratinocytes were treated with ultraviolet-B, ultraviolet-A, or sham irradiation, without or with exogenous interleukin-12. Remarkably, the exogenous interleukin-12 totally blocked ultraviolet-B-induced tumor necrosis factor alpha production. Both ultraviolet-A and ultraviolet-B were capable of inducing interleukin-12 production. To determine the molecular mechanism of this effect, we used a chloramphenicol acetyl transferase reporter under the control of a 1.2 kb fragment of the wild-type (-308G) human tumor necrosis factor alpha promoter and found significant suppression of promoter activity with interleukin-12. Studies using the -308A variant of the human tumor necrosis factor alpha promoter showed much higher promoter activity overall, but also a greater sensitivity to suppression by interleukin-12. The mechanism did not involve blockage of the interleukin-1 receptor, because interleukin-12 did not suppress interleukin-1-mediated induction of collagenase mRNA. To determine the role of endogenous interleukin-12, we found that anti-interleukin-12 antibodies enhanced ultraviolet-B-induced tumor necrosis factor alpha secretion. Thus, interleukin-12 strongly inhibits tumor necrosis factor alpha production by noninflammatory skin cells, mostly or entirely through inhibition of gene transcription via an element within the first 1.2 kb of the tumor necrosis factor alpha promoter. The result is a shift in tumor necrosis factor alpha production from noninflammatory cells to T helper 1 cells. Because tumor necrosis factor alpha is central to the pathogenesis of several photosensitive skin diseases and certain forms of immune suppression, interleukin-12 may have important physiologic, pathophysiologic, and therapeutic roles.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12535207&dopt=Abstract
Osteoarthritis Cartilage. 2002 Nov;10(11):838-44.
T(1rho) relaxation can assess longitudinal proteoglycan loss from articular cartilage in vitro.
Duvvuri U, Kudchodkar S, Reddy R, Leigh JS.
Department of Radiology, University of Pennsylvania, Philadelphia 19104, USA. uduvvurail.mmrrcc.upenn.edu
Objective To assess the correlation between changes in spin-lattice relaxation in the rotating frame (T(1rho)) and proteoglycan (PG) loss from bovine articular cartilage and to demonstrate the feasibility of performing T(1rho) MR imaging on a 1.5T clinical scanner.Design MR relaxation times (T(1rho), T(2) and T(1)) were measured from excised cartilage plugs (N=3) before and after two sequential digestions with trypsin on a 2T whole-body magnet. Proteoglycan and collagen loss induced by the trypsin digestion was measured using standard biochemical techniques. The correlation between changes in relaxation times and PG loss were tested with regression analysis. T(1rho) MRI was also performed on a clinical 1.5T MRI system to determine whether the spatial distribution of PG loss could be detected. The MRI results were compared with histology sections of native and PG-depleted tissue.Results Increase in T(1rho) relaxation times correlated with PG loss (R(2)=0.81). T(1rho) measurements alone were indicative of PG loss (R(2)=0.8), the addition of T1 and T2 data into the statistical model did not improve the correlation substantially (R(2)=0.83). T(1rho)-weighted imaging demonstrated a hyperintense lamina at the articular surface of the digested tissue, which was subjected to trypsin digestion that correlated with a superficial zone of PG loss observed on histological sections.Conclusion The results of this study demonstrate that T(1rho) relaxation changes are correlated with PG loss in vitro. Furthermore, T(1rho) measurements alone can be used to indicate PG loss data. T(1rho) MRI may thus be developed into a useful adjunct to existing techniques for the evaluation of cartilage disease. 2002 OsteoArthritis Research Society International. Published by Elsevier Science Ltd.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12435327&dopt=Abstract
Zhonghua Gan Zang Bing Za Zhi. 2000 Oct;8(5):299-301.
Effects of carbon tetrachloride-injured hepatocytes on hepatic stellate cell activation and salvianolic acid A preventive action in vitro.
[Article in Chinese]
Hu Y, Wang R, Zhang X, Liu C, Liu C, Liu P, Zhu D.
Institute of Liver Diseases, Shanghai University of Traditional Chinese Medicine, Shanghai 200032, China.
OBJECTIVE: To investigate the effects of carbon tetrachloride (CCl(4))-injured hepatocyte on hepatic stellate cell (HSC) activation, the relation between lipid peroxidation and liver fibrosis, and the action mechanisms of salvianolic acid A (SA-A), one of water soluble components extracted from radix salvia miltiorrhizae, against HSC activation and liver fibrosis. METHODS: The hepatocytes were isolated from the normal rats, incubated with SA-A at different concentrations, respectively, and vitamin E severed as control. At the same time the cells were fumigated with CCl(4) for 24h, and ALT activities in the medium were measured. After the cell medium was changed and cultured for another 24h, the medium was collected as "hepatocyte conditioned medium" (HCM) and measured for malondiadehyde (MDA) content. Then HCM was incubated with primary cultured HSC for 48h, and HSC proliferation, type I collagen gene expression and protein production were observed. RESULTS: ALT activity and MDA content in the hepatocyte medium were increased remarkably after the cell was injured. HCM could obviously promote HSC proliferation, type I collagen mRNA expression and protein production. SA-A could markedly inhibit ALT activity and MDA content in hepatocytes, and decreased collagen gene expression and protein production. CONCLUSION: The secretion from the peroxidative injured hepatocyte could stimulate HSC activation, SA-A could decrease activation by alleviation of hepatocyte peroxidation.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11058958&dopt=Abstract
Zhonghua Gan Zang Bing Za Zhi. 2000 Oct;8(5):302-4.
Effects of angiotensin II receptor blockade on hepatic fibrosis in rats.
[Article in Chinese]
Wei H, Li D, Lu H, Zhan Y, Wang Z, Huang X, Pan Q, Xu Q.
Department of Gastroenterology, Xinhua Hospital, Shanghai Second Medical University, Shanghai 200092, China.
OBJECTIVE: To investigate the effects of angiotensin II type 1 receptor blockade, losartan, on serum levels of components of extracellular matrix in experimental fibrotic rats. METHODS: Fifty male Spague-Dawley rats were separated into five groups (control, model, and 3 treatment groups). Excepting rats in control group, all rats were given subcutaneous injection of 40% carbon tetrachloride (once every 3 days for 6 weeks). Rats in 3 treatment groups were also given losartan of 10mg/kg, 5mg/kg, 2.5mg/kg daily for 6 weeks via gastrogavage, respectively. At the end of sixth week, all rats were sacrificed. Radioimmunoassay was performed to determine the serum levels of hyaluronic acid (HA), Laminin (LN), procollagen type III (PCIII) and collagen type IV. Van Giesion collagen staining was used to evaluate the extracellular matrix of the liver tissue. RESULTS: Compared with model group, losartan significantly reduced the serum levels of HA [from (911.66 +/- 345.49)microg/L to (425.05 +/- 115.80)microg/L], LN [from (209.87 +/- 91.57)microg/L to (83.56 +/- 22.12)microg/L, PCIII [from (31.82 +/- 6.90)microg/L to (22.78 +/- 8.38)microg/L] and collagen IV [from (54.09 +/- 19.81)microg/L to (30.51 +/- 12.39)microg/L] (P<0.05) and greatly attenuated the degree of liver fibrosis (P<0.05). CONCLUSION: Losartan can markedly reduce the serum levels of LN, HA, PCIII and collagen type IV of fibrotic rats induced by CCl(4) and greatly attenuate the degree of liver fibrosis.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11058959&dopt=Abstract
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