Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “CD44”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 631 records · Page 35Linked to original sources
PubMed2002

Expression of cadherins and CD44 isoforms in human endometrium and peritoneal endometriosis.

BACKGROUND: To evaluate (a) cadherins and CD44 expression in normal endometrium and in peritoneal endometriosis, and (b) to correlate, their expressions with clinicopathological parameters. METHODS: E- and N-cadherin, CD44 isoforms, CD44v3 and CD44v6 expressions were evaluated: (a) by immunoblotting in endometrium (n = 6) and in peritoneal endometriotic samples (n = 7) and, (b) by immunohistochemistry in endometrium (n = 15) and in peritoneal endometriotic samples (n = 23). RESULTS: By immunoblotting, endometrium expressed E- and N-cadherin, CD44 isoforms, CD44v3 and CD44v6. Similar results were observed in peritoneal endometriosis. By immunohistochemistry, in endometrium, E-cadherin was restricted to epithelial cells. Its expression remained constant throughout the menstrual cycle. N-cadherin was detected in both epithelial and stromal cells in the proliferative phase but was restricted to epithelial cells in the secretory phase. CD44 immunostaining was detected in the secretory but not in the proliferative phase. Decreased expression of E-cadherin (p < 0.01) and CD44 (p < 0.01) in epithelial cells was found in peritoneal endometriosis as compared with normal endometrium. In endometriotic stromal cells, decreased CD44 expression was found. In peritoneal endometriosis, we observed a decreased expression of E-cadherin in advanced stages of the disease (p < 0.01). CONCLUSION: Our results suggest that E-cadherin and CD44 proteins could be involved in the development of endometriotic lesions. Investigation of the mechanisms of altered adhesion molecule expression may contribute to the understanding of the behavior of endometriotic cells.

Adult↗
PubMed2002

Expression of CD44 and CD44v6 in primary cutaneous CD30 positive T-cell lymphoproliferative disorders.

BACKGROUND: Expression of the lymphocyte homing receptor CD44 and its variant form, CD44v6, have been linked to unfavorable prognosis and tumor dissemination in non-Hodgkin's lymphoma. The role of CD44 and CD44v6 in primary cutaneous lymphomas may not necessarily correlate with that observed in nodal lymphomas. Our study attempts to evaluate the expression pattern of CD44 and CD44v6 in primary cutaneous CD30 positive T-cell lymphoproliferative disorders including primary cutaneous anaplastic large cell lymphoma (cALCL) and lymphomatoid papulosis (LyP) and compared the expression between these two subgroups. METHODS: Immunohistochemical staining of CD44 and CD44v6 was performed on 10 cALCL and 18 LyP cases. RESULTS: CD44 consistently expressed in all cases of primary cutaneous CD30 positive T-cell lymphoproliferative disorders. In contrast with previous studies, our results showed that CD44v6 expressed in 46% of all cases, including 50% cALCL and 44% LyP. There was no statistic difference in expression of CD44 or CD44v6 between cALCL and LyP subgroups. CONCLUSIONS: These results provide a new evidence that CD44v6 is expressed in a subset cases of primary cutaneous CD30 positive T-cell lymphoproliferative disorders and suggest that other factors or molecules rather than CD44 or CD44v6 are responsible for the difference between cALCL and LyP.

Adult↗
PubMed1998

The prognostic value of CD44 isoform expression in endometrial cancer.

Isoforms of the transmembrane glycoprotein CD44 have been implicated in tumour cell adhesion, tumour differentiation and metastatic spread in various human malignancies. We investigated the expression of CD44 isoforms containing variant exons v3, v5, v6 and v7-8 in 156 human endometrium cancer specimens by means of immunohistochemistry. CD44 isoforms CD44v3, CD44v5, CD44v6 and CD44v7-8 were detected in 26% (41 out of 156), 31% (48 out of 156), 22% (35 out of 156) and 15% (23 out of 156) of the tumour samples respectively. The expression of CD44 isoforms CD44v3, CD44v5 and CD44v7-8 showed no prognostic impact. In the univariate analysis, the expression of CD44v6 showed an association with shortened overall survival (log-rank test, P = 0.06). Multivariate analysis correcting for the confounding variable histological grading revealed CD44v6 not to be a prognostic factor in endometrial cancer (log-rank test, P = 0.06). Comparing the expression of CD44 isoforms CD44v3, CD44v5, CD44v6 and CD44v7-8 in 45 specimens of normal endometrial tissue, we found an up-regulation of all investigated CD44 isoforms in the secretory phase compared with the proliferative phase of the menstrual cycle. Our data indicate that the expression of CD44 isoforms, while obviously playing a role in the functional changes of normal endometrium, is not an adverse predictive factor in endometrial cancer.

Aged↗
PubMed1996

CD44 in glomerulonephritis: expression in human renal biopsies, the Thy 1.1 model, and by cultured mesangial cells.

CD44 is a transmembrane proteoglycan that serves as a cell adhesion receptor and is involved in cell-cell and cell-matrix interactions, both key events in the pathogenesis of clinical and experimental glomerulonephritis. In addition, recent evidence suggests that the binding of cytokines to proteoglycans could regulate cytokine function. We have, therefore, studied the expression of CD44 by mesangial cells in culture and in experimental (Thy 1.1 model) and human glomerulonephritis. Mesangial expression of CD44 detected by immunohistochemistry was markedly increased four days after induction of the Thy 1.1 model, coinciding with the peak of mesangial cell proliferation and macrophage infiltration. Analysis of 92 human renal biopsies by immunohistochemistry showed that CD44 expression by infiltrating cells within the glomerulus, in focal interstitial infiltrates and within the interstitium (interstitial fibroblasts, and extracellular matrix), was significantly increased in biopsies with a greater degree of histological damage. There was, however, no increase in mesangial staining in diseased kidneys as compared with control sections. In contrast, cultured human mesangial cells expressed CD44 strongly when assayed by immunohistochemistry, immunoprecipitation and Northern blotting. CD44, therefore, is an example of a protein strongly expressed by mesangial cells in vitro and weakly or not at all in vivo, but which is up-regulated in a disease model. In human disease, however, little expression was detected within the glomerular mesangium, which may be related to the greater proliferation and more profound disruption of mesangial architecture seen in the Thy 1.1 model. CD44 expression by infiltrating cells and by components of the interstitium could, however, play an important role in the pathogenesis of chronic progressive renal disease in humans.

Animals↗
PubMed2006

Renal expression of CD44 correlates with acute renal allograft rejection.

As CD44 is involved in the activation, proliferation, adhesion, and extravasation of lymphocytes, we hypothesized that CD44 could be involved in the pathogenesis of acute renal allograft rejection. Renal biopsies and plasma were collected from patients suffering an episode of acute renal allograft rejection. CD44 and its ligands, hyaluronic acid (HA) and osteopontin, were analyzed retrospectively by immunohistochemistry and, computer-aided, morphometric analysis. Soluble CD44 (sCD44) and osteopontin in the plasma were determined by enzyme-linked immunosorbent assay. During acute rejection episodes, CD44 and its ligands, HA and osteopontin, were upregulated in the renal allograft. Also, increased sCD44 plasma levels were observed, which correlated with both tubular expression of CD44 and the extent of infiltrate. No differences could be detected between the different pathologic grades of rejection. Upregulation of tubular CD44 and increased levels of circulating sCD44 may reflect a common pathogenic mechanism during acute renal rejection and could be useful markers in the diagnosis of acute renal rejection.

Acute Disease↗
PubMed1997

Activation of beta1 integrins on CML progenitors reveals cooperation between beta1 integrins and CD44 in the regulation of adhesion and proliferation.

Adhesion of normal colony-forming cells (CFC) to bone marrow (BM) stroma and the extracellular matrix (ECM) component fibronectin (FN) depends at least in part on the alpha4beta1 and alpha5beta1 integrins and the CD44 receptor. Aside from anchoring progenitors in the marrow microenvironment, beta1 integrin-dependent adhesion of normal CFC is associated with inhibition of their proliferation. In contrast to normal CFC, chronic myelogenous leukemia (CML) Ph+ CFC adhere significantly less to either stroma or FN. CML Ph+ CFC proliferation is also not inhibited by coculture with stroma or FN. However, equal numbers of alpha4, alpha5, and beta1 integrins and CD44 are present on CML and normal CD34+ cells. We have previously demonstrated that beta1-dependent adhesion to and subsequent proliferation inhibition by FN can be restored when CML Ph+ CFC are incubated with the beta1 integrin activating antibody, 8A2, and demonstrated a role for the alpha5beta1 integrin in this phenomenon. Since the integrin alpha4beta1 and the proteoglycan form of CD44 may cooperate in establishing normal CFC adhesion to FN, we examined if treatment of CML Ph+ CFC with 8A2 also restores the cooperativity between beta1 integrins and CD44. We demonstrate that 8A2 induces adhesion of CML Ph+ CFC not only to intact FN but also to alpha4beta1, alpha5beta1, and proteoglycan binding fragments of FN. 8A2-induced adhesion to these fragments and peptides also results in a significant inhibition of the proliferation of CML Ph+ CFC. Addition of antibodies to either the alpha5, alpha4, or beta1 integrins, antibodies against the CD44 receptor, or removal of chondroitin sulfate glycosaminoglycans from the surface of CML CD34+ HLA-DR+ cells significantly reduced the 8A2-induced adhesion to and adhesion-mediated inhibition of proliferation by FN. These studies demonstrate that activation of beta1 integrins on CML Ph+ CFC not only results in upregulation of beta1 integrin-dependent adhesion and adhesion-mediated inhibition of proliferation, but also in the restoration of cooperation between beta1 integrins and CD44. These studies suggest that decreased beta1 integrin avidity may also affect the function of the proteoglycan adhesion receptor CD44, both of which may contribute to the abnormal circulation and expansion of malignant progenitors in CML.

Antigens, CD↗
PubMed1997

Expression of CD44 isoforms in neuroblastoma cells is regulated by PI 3-kinase and protein kinase C.

With respect to a potential role for CD44 in neuronal tumors, we investigated the regulation of variant CD44 exon containing isoforms (CD44V) in the human neuroblastoma cell line SK-N-SH in response to treatment with differentiation-inducing and mitogenic factors. While the standard form of CD44 was expressed at high levels in both treated and untreated cells, variant isoforms were strongly upregulated in response to treatment with 12-O-tetradecanoyl phorbol-13-acetate (TPA), insulin-like growth factor-1 (IGF-1) and platelet-derived growth factor (PDGF) as shown by RT-PCR and immunofluorescence. One of the CD44 isoforms contains sequences encoded by variant exon v6 (CD44V6), which was originally described as a metastasis-associated antigen. Using specific inhibitors, we explored the signal transduction pathways involved in the expression of variant CD44. GF-109203X, a specific inhibitor of protein kinase C effectively blocked TPA- and IGF-1-upregulated expression of CD44v6. Wortmannin, a specific inhibitor of phosphoinositide 3-kinase (PI 3-kinase) partly reduced IGF-1 and PDGF induced CD44v6 expression. The induction of CD44V by TPA, IGF-1 or PDGF was correlated with an increased cellular binding to hyaluronic acid, a major counterreceptor for CD44. The increased binding caused by TPA or IGF-1 could specifically be blocked by the above inhibitors. Thus, PKC and PI 3-kinase are likely to transduce growth factor induced signals that upregulate specific CD44 splice variants.

Carcinogens↗
PubMed2004

Recombinant CD44-HABD is a novel and potent direct angiogenesis inhibitor enforcing endothelial cell-specific growth inhibition independently of hyaluronic acid binding.

CD44 is the main cellular receptor for hyaluronic acid (HA). We previously found that overexpression of CD44 inhibited tumor growth of mouse fibrosarcoma cells in mice. Here, we show that soluble recombinant CD44 HA-binding domain (CD44-HABD) acts directly onto endothelial cells by inhibiting endothelial cell proliferation in a cell-specific manner. Consequently, soluble recombinant CD44-HABD also blocked angiogenesis in vivo in chick and mouse, and thereby inhibited tumor growth of various origins at very low doses (0.25 mg/kg x day). The antiangiogenic effect of CD44 is independent of its HA-binding capacity, since mutants deficient in HA binding still maintain their antiangiogenic and antiproliferative properties. Recombinant CD44-HABD represents a novel class of angiogenesis inhibitors based on a cell-surface receptor.

Angiogenesis Inhibitors↗
PubMed2006

Cortactin underpins CD44-promoted invasion and adhesion of breast cancer cells to bone marrow endothelial cells.

Using a validated tetracycline (tet)-regulated MCF7-founder (MCF7F) expression system to modulate expression of CD44 standard form (CD44s), we report the functional importance of CD44s and that of a novel transcriptional target of hyaluronan (HA)/CD44s signaling, EMS1/cortactin, in underpinning breast cancer metastasis. In functional experiments, tet-regulated induction of CD44s potentiated the migration and invasion of MCF7F cells through HA-supplemented Matrigel. EMS1/cortactin was identified by expression profiling as a novel transcriptional target of HA/CD44 signaling, an association validated by quantitative PCR and immunoblotting experiments in a range of breast cancer cell lines. The mechanistic basis underpinning CD44-promoted transcription of EMS1/cortactin was shown to be dependent upon a NFkappaB mechanism, since pharmacological inhibition of IkappaKinase-2 or suppression of p65 Rel A expression attenuated CD44-induced increases in cortactin mRNA transcript levels. Overexpression of a c-myc tagged murine cortactin construct in the weakly invasive, CD44-deficient MCF7F and T47D cells potentiated their invasion. Furthermore, the functional importance of cortactin to CD44s-promoted metastasis was demonstrated by selective suppression of cortactin in CD44-expressing MCF7F-B5 and MDA-MB-231 breast cancer cells using RNAi, which was shown to result in attenuated CD44-promoted invasion and CD44-promoted adhesion to bone marrow endothelial cells (BMECs).

Base Sequence↗
PubMed1999

The expression of CD44 glycoprotein adhesion molecules in basal cell carcinomas is related to growth pattern and invasiveness.

Basal cell carcinomas (BCCs) of the skin exhibit a wide range of histological growth patterns as well as a highly variable rate of invasiveness. A large body of experimental and clinical studies supports a role for the CD44 glycoprotein family in the latter process. In the present study, we explored the distribution and the level of expression of pan-CD44, CD44v3, CD44v5 and CD44v6 in BCCs. The use of paraffin sections, combined with an antigen retrieval procedure, yielded far more detailed data than would have been possible with frozen sections. On average, the level of expression of the four CD44 isoforms studied appeared to differ relatively little. However, tumours or tumour areas consisting of thin tumour cell strands showed a significantly stronger expression of all four isoforms than those consisting of solid tumour cell groups. Furthermore, the highest CD44 expression was frequently observed in the smallest tumour cell strands in the tumour periphery. In these strands, the label seemed to be located not only at the tumour cell-tumour cell interface, as in other tumour areas, but also on the tumour cell surfaces facing the stroma. We are presently assessing the exact localization of CD44 at the cellular level by immunoelectron microscopy. In most cases, different growth patterns with significantly different levels of CD44 expression were found side by side within individual tumours. CD44 expression is therefore not a static tumour cell characteristic but is correlated with tumour architecture and tumour-stroma interaction.

Actins↗
PubMed2001

Expression of CD44 and its variant isoform v3 has no prognostic value in gastric cancer.

AIMS: To study the controversial role of transmembrane glycoprotein CD44 as a moderator of tumour spread and as a prognostic factor in gastric cancer. METHODS AND RESULTS: The expression of all CD44 forms and that with exon v3 was assessed in 198 stage I-IV gastric adenocarcinomas using immunohistochemistry. CD44 expression was found in 72% and CD44v3 in 55% of the cases. The intensity of CD44 expression was associated with the level of invasion and with hyaluronan expression, while the frequency of CD44 positive cells was not significantly related to any of the clinical or histological features of the tumours. CD44v3 expression failed to show any association with the clinical or histological variables examined. Neither total CD44 nor CD44v3 expression affected survival. The most important prognostic factors in this cohort were the level of invasion, lymph node status, tumour size and vascular or perineural invasion. CONCLUSIONS: Changes in CD44 or CD44v3 expression level do not predict tumour spread or patient survival in gastric cancer.

Adenocarcinoma↗
PubMed2000

Induction of interactions between CD44 and hyaluronic acid by a short exposure of human T cells to diverse pro-inflammatory mediators.

Migration of T cells into extravascular sites of inflammation is mediated by cell-cell and cell-matrix adhesion receptors, including the hyaluronan-binding glycoprotein, CD44. The biochemical nature of CD44 variants and the ligand specificity, function and the regulation of activation of CD44 expressed on various cell types have been extensively studied. However, little is still known about the short-term influence of cytokines and chemokines on the activation of CD44 on human T cells. Therefore, we studied the role of inflammatory mediators in regulating the adhesion of T cells from human peripheral blood to immobilized hyaluronan under static or shear stress conditions. We found that the CD44-dependent adhesion, under static and shear stress (i.e. relative gradual resistance to flow of 150 and 1500 s-1) conditions, of T cells to hyaluronan requires a T-cell activation of 2-3 hr and is regulated by the cross-linking of CD3, cytokines (e.g. interleukin-2 and tumour necrosis factor-alpha), and chemokines (e.g. MIP-1beta, interleukin-8, and RANTES). This T-cell adhesion was manifested by polarization, spreading and co-localization of cell surface CD44 with a rearranged actin cytoskeleton in hyaluronan-bound T cells. Thus, cytokines and chemokines present in the vicinities of blood vessel walls or present intravascularly in tissues where immune reactions take place, can rapidly activate the CD44 molecules expressed on T cells.

Antibodies, Monoclonal↗
PubMed1996

Transient expression of CD44 variant isoforms in the ontogeny of the rat: ectoderm-, endoderm- and mesoderm-derived cells express different exon combinations.

Expression on rat tumor cells of CD44 variant isoforms containing exons v4-v7 or v6-v7 has been described as sufficient for initiation of the metastatic cascade. The question arose as to whether physiological programs may be reactivated by particular CD44 isoforms. With this in mind, expression of mRNAs for the CD44 isoforms was surveyed during ontogeny of the rat. Using available monoclonal antibodies, expression of the CD44 standard isoform (CD44s) and of an epitope of CD44 exon v6 (CD44v6) were evaluated by immunohistology also. While CD44s was expressed in cells of all three germ layers, CD44v6 expression was restricted to distinct epithelial layers and cells of the hematopoietic system. During ontogeny, expression of CD44v6 was first noted in the neural tube and the leading epithelial layer of the limb buds. Later, anti-CD44v6 (1.1ASML) stained basal layers of the epidermis, the epithelium of the gut, and the acini of the submandibular gland. Strong, but transient expression of CD44v6 was seen during lung development, in hematopoietic stem cells of the liver, in thymic epithelia and early thymic immigrants. Expression in these organs was downregulated shortly before or after birth. As revealed by Southern blotting after use of the reverse transcriptase polymerase chain reaction (RT-PCR), most CD44v6-positive organs contained more than one CD44 variant isoform, and the expression patterns differed between individual organs. Hematopoietic cells preferentially expressed exons v4-v7, endodermal tissue exons v4-v10 and only in the epidermis were exons v1-v10 detected. The temporally regulated expression during ontogeny and the different exon compositions suggest a pivotal role of CD44 isoforms particularly in hematopoesis and in pattern formation by instructive epithelia.

Animals↗
PubMed2000

Interaction between hyaluronan and CD44 in the development of dimethylnitrosamine-induced liver cirrhosis.

BACKGROUND: A significant increase in serum hyaluronan (HA) levels has been reported in patients with liver cirrhosis. This mechanism is not yet clear, and receptors for HA have not been characterized. In this study, we examined the expression of both HA and its receptors, CD44 and intercellular adhesion molecule-1 (ICAM-1), in dimethylnitrosamine-induced liver cirrhosis. METHODS AND RESULTS: Using biotinylated HA binding protein, HA was detected in the area of periportal fibrosis and around the sinusoidal wall where hepatic fibrosis was developing. Electron microscopy revealed that HA was localized on Ito cells and sinusoidal endothelial cells (SEC). Conversely, CD44, which was only expressed weakly in normal liver, was present in large amounts in cirrhotic liver. The distribution pattern of CD44 was similar to that of HA, however, CD44 was mainly localized on the infiltrating lymphocytes and Kupffer cells. Moreover, CD44 was detected on part of factor VIII-positive SEC. Intercellular adhesion molecule-1, another receptor for HA, was detected on the surface of hepatocytes and around the sinusoidal wall in cirrhotic liver, but its distribution was not accompanied by expression of HA. With respect to CD44 isoforms, the standard form m-RNA predominated in both normal and cirrhotic liver. Variant pMeta-1 mRNA was detected at low levels. CONCLUSIONS: An interaction between HA and CD44 may play a role in the recruitment of numerous infiltrating cells and HA accumulation in hepatic sinusoids. Together with phenotypic changes in the SEC, these results may lead to a disturbance in the elimination of HA during the progression of liver cirrhosis.

Animals↗
PubMed2001

Serum levels and differential expression of CD44 in childhood leukemia and malignant lymphoma: correlation with prognostic criteria and survival.

BACKGROUND: The CD44, a cell surface proteoglycan, participates in a variety of function including tumor dissemination and metastasis. However, there are no available data on the prognostic significance of CD44 expression of tumor tissue correlated with serum sCD44 level in childhood leukemias and lymphomas. METHODS: Serum levels and leukemic cell tumor tissue expression of CD44 were detected in 54 children with acute leukemia and malignant lymphoma. Serum samples were obtained from all patients before treatment and during remission. Twelve age-matched healthy children were included as a control group. RESULTS: The serum CD44 levels were significantly higher in patients with Hodgkin's disease (HD), non-Hodgkin's lymphoma (NHL), Burkitt's lymphoma (BL) and acute lymphoblastic leukemia (ALL) than those in the control group. The median values were 1627.0, 1336.0, 1318.5, 1730.4, 902.7 ng/mL, respectively, and P<0.001, P<0.01, P<0.01, P<0.05 in comparisons, respectively. However, there was no significant difference between acute myeloid leukemia (AML) and the control group (median values: 900.3 and 902.7 ng/mL, respectively, P>0.05). Serum sCD44 levels significantly declined in HD, NHL and ALL patients who were in complete remission (median values: 684.0, 573.8 and 1101.1 ng/mL, respectively, P<0.05 in each comparison). Patients with HD had higher levels of serum sCD44 and correlated well with higher erythrocyte sedimentation rate (ESR), B-symptoms and advanced-stage disease (P<0.05, P<0.05 and P<0.01, respectively). Expression of CD44 was significantly high in patients with HD and NHL who were in advanced stages of disease. High serum CD44 level was also associated with high tumor tissue expression of CD44 in patients with HD and BL. In addition, patients with higher levels of serum sCD44, had a poorer outcome and survival than those with lower sCD44 levels in HD and NHL groups. CONCLUSIONS: A high serum sCD44 level and/or tumor tissue expression at diagnosis is associated with poor prognostic criteria and/or unfavorable outcome in childhood leukemias and lymphomas.

Adolescent↗
PubMed2003

Perturbation of CD44 function affects chiasmatic routing of retinal axons in brain slice preparations of the mouse retinofugal pathway.

Neurons generated early in development of the ventral diencephalon have been shown to play a key role in defining the midline and the caudal boundary of the optic chiasm in the mouse retinofugal pathway. These functions have been attributed to a surface bound adhesion molecule, CD44 that is expressed in these chiasmatic neurons. In this study, we investigated the effects of perturbing normal CD44 functions on axon routing in brain slice preparations of the mouse retinofugal pathway. Two CD44 antibodies (Hermes-1 and IM7) were used that bind to distinct epitopes on the extracellular domain of the molecule. We found that both antibodies produced dramatic defects in routing of the retinal axons that arrive early in the chiasm. In preparations of embryonic day 13 (E13) and E14 pathways, the crossed component in the chiasm was significantly reduced after antibody treatment. However, such reduction in axon crossing was not observed in E15 chiasm, indicating that the lately generated crossed axons lost their responses to CD44. Furthermore, the anti-CD44 treatment produced a reduction in the uncrossed component in the E15 but not in younger pathways, suggesting a selective response of the lately generated axons, mostly from ventral temporal retina, but not those generated earlier, to the CD44 at the chiasmatic midline in order to make their turn for the uncrossed pathway. These findings provide evidence that a normal function of CD44 molecules in the chiasmatic neurons is essential for axon crossing and axon divergence at the mouse optic chiasm.

Animals↗
PubMed2002

CD44 expression in IgA nephropathy.

Immunoglobulin A (IgA) nephropathy is a frequent, chronic renal disease characterized by a broad spectrum of clinical presentations and pathologic findings. CD44, a family of type I transmembrane glycoproteins involved in cell-cell and cell-matrix interactions, may orchestrate partially the cascade of inflammation, accumulation of myofibroblasts, and fibrosis leading to end-stage renal disease. To clarify the possible role of CD44 in the progression of IgA nephropathy, the expression of CD44 in glomeruli and the tubulointerstitial compartment was analyzed in 25 renal biopsy specimens of patients with IgA nephropathy and was correlated to histopathologic, serologic, and urinary parameters. The expression of CD44 correlated significantly with the degree of glomerular and interstitial damage, even better than the accumulation of alpha-smooth muscle actin-positive myofibroblasts, which is recognized as a reliable marker for the progression of IgA nephropathy. A positive correlation also was found between proteinuria and the expression of CD44 in the tubulointerstitial compartment. The glomerular and tubulointerstitial expression of CD44 correlated with the degree of renal damage in IgA nephropathy and could be a reliable marker of the progression of IgA nephropathy. CD44 may have a pivotal role in the cascade of renal inflammation and fibrosis.

Adult↗
PubMed1996

Expression of variant CD44-messenger RNA in colorectal adenocarcinomas and adenomatous polyps in humans.

BACKGROUND & AIMS: Recent studies have shown that some variant forms of CD44, a transmembrane glycoprotein expressed on various cell surfaces, might be involved in tumor progression or tumor metastasis. The aim of this study was to analyze the expression of CD44-messenger RNA (mRNA) in colorectal cancer and colorectal adenoma to further elucidate the role of CD44 in colorectal tumorigenesis. METHODS: The expression of CD44-mRNA was examined in 90 specimens from 44 patients with colorectal cancer or colorectal adenomatous polyps and in the peripheral blood leukocytes from 7 healthy volunteers by reverse transcription-polymerase chain reaction and Southern blot hybridization. RESULTS: Strong expression of the epithelial form and variant forms containing exons 11 or 12 of the CD44 gene, which conferred metastatic behavior to rat cells, was detected in primary and metastatic tumor tissues, whereas it was very weak or not detectable in normal colonic mucosae, normal liver tissue, or peripheral blood leukocytes. However, adenomatous colorectal polyps also showed as strong an expression of epithelial and variant forms of CD44 as primary and metastatic tumor tissues. CONCLUSIONS: These results suggest that variant forms of CD44-mRNA might be expressed in an early stage of colorectal carcinogenesis.

Adenocarcinoma↗