Osp/Claudin-11 Forms a Complex with a Novel Member of the Tetraspanin Super Family and β1 Integrin and Regulates Proliferation and Migration of Oligodendrocytes

Tiwari‐Woodruff, Seema K.; Buznikov, Alex G.; Vu, Trung; Micevych, Paul E.; Chen, Kendall; Kornblum, Harley I.; Bronstein, Jeff M.

doi:10.1083/jcb.153.2.295

Cited by 173 publications

(141 citation statements)

References 65 publications

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“…Interestingly, claudins have been shown to interact with tetraspanin molecules. For example, claudin-11 interacts with OAP-1 to form a complex with integrins, which results in increased oligodendrocyte proliferation and migration (Tiwari-Woodruff et al, 2001). In addition, claudin-7 has been shown to form a complex with tetraspanins, EpCam and CD44 in colorectal cancers, and expression of these molecules was inversely correlated with disease-free survival (Kuhn et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

Claudin-2 is selectively enriched in and promotes the formation of breast cancer liver metastases through engagement of integrin complexes

et al. 2010

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The liver represents the third most frequent site of metastasis in patients with breast cancer. We performed in vivo selection using 4T1 breast cancer cells to identify genes associated with the liver metastatic phenotype. Coincident with the loss of numerous tight-junctional proteins, we observe claudin-2 overexpression, specifically in liver-aggressive breast cancer cells. We further demonstrate that claudin-2 is both necessary and sufficient for the ability of 4T1 breast cancer cells to colonize and grow in the liver. The liver-aggressive breast cancer cells display a claudin-2-mediated increase in their ability to adhere to extracellular matrix (ECM) components, such as fibronectin and type IV collagen. Claudin-2 facilitates these cell/matrix interactions by increasing the cell surface expression of a 2 b 1 -and a 5 b 1 -integrin complexes in breast cancer cells. Indeed, claudin-2-mediated adhesion to fibronectin and type IV collagen can be blocked with neutralizing antibodies that target a 5 b 1 and a 2 b 1 complexes, respectively. Immunohistochemical analyses reveal that claudin-2, although weakly expressed in primary human breast cancers, is readily detected in all liver metastasis samples examined to date. Together, these results uncover novel roles for claudin-2 in promoting breast cancer adhesion to the ECM and define its importance during breast cancer metastasis to the liver.

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Section: Discussionmentioning

confidence: 99%

Claudin-2 is selectively enriched in and promotes the formation of breast cancer liver metastases through engagement of integrin complexes

et al. 2010

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“…Interestingly, altered TFN expression has been associated with schizophrenia and expression of TFN and MBP during development has been reported delayed in animals following chronic ethanol treatment [29,38,63]. CLDN11 is a developmentally regulated protein that is expressed in interlamellar strands of myelin sheaths [64,65], and is involved in establishment of tight-junctions in myelinating cells and has overlapping functions with PLP1 in maintaining myelin's structural integrity [66][67][68][69]. Based on these functions, decreased CLDN11 and TFN expression could compromise myelin function and structural integrity.…”

Section: Discussionmentioning

confidence: 99%

Expression of Transcripts for Myelin Related Genes in Postmortem Brain from Cocaine Abusers

2008

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Chronic abuse of cocaine is known to cause neuroadaptive changes in the nucleus accumbens (NAc) and ventral tegmental area (VTA). In addition, altered expression of the myelin-related genes MBP, MOBP, PLP1 as well as of MAL2 in NAc was recently reported by gene array analysis in brains from cocaine abusers. In the present study we used in situ hybridization to quantify transcript expression of these four genes, as well as for the myelin-related transcripts encoding quaking, EDG2, claudin-11, transferrin, CNP, and MAG in caudate, putamen, internal capsule, and NAc in postmortem brain from cocaine abusers and matched comparison subjects. Most transcripts were not different between these groups in these striatal regions, and contrary to previous reports, we did not detect any changes in the NAc. However, expression of the transcript encoding PLP1 was significantly decreased in ventral and dorsal regions of the caudate, putamen, and in the internal capsule. Additionally, expression of claudin-11 and transferrin was decreased in the caudate and internal capsule, respectively. PLP1 is expressed at very high levels in oligodendrocytes and is essential in maintaining stability of myelin sheets. Based on these findings, altered expression of PLP1 in most areas of the striatum suggests that widespread changes to the myelin structure could be associated with the adaptive changes following chronic cocaine abuse.

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“…OSP is a 207-aa, four-membrane spanning protein with considerable hydrophobic character that forms tight junctions within myelin sheaths [17,18]. OSP is primarily expressed in oligodendrocytes of the CNS and in Sertoli cells of testes [19][20][21]. Experiments in rodents have established that immunoreactivity to OSP induces experimental autoimmune encephalomyelitis (EAE), and suggest a pathogenic potential for autoreactive T cells recognizing OSP in MS patients [22][23][24][25][26].…”

Section: Introductionmentioning

confidence: 99%

Oligodendrocyte‐specific protein is encephalitogenic in rhesus macaques and induces specific demyelination of the optic nerve

et al. 2008

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Oligodendrocyte-specific protein (OSP) is a candidate autoantigen in the development of multiple sclerosis (MS). We evaluated the potential of OSP to induce EAE in rhesus monkeys, an out bred animal model for MS that is immunologically close to humans. Since OSP is a four-membrane spanning protein with highly hydrophobic regions, we synthesized recombinant proteins encompassing only the hydrophilic regions of human OSP (soluble (s)hOSP). Immunization with shOSP proteins induced clinical signs and histological features of optic neuritis in four out of ten rhesus monkeys. The development of clinical disease was associated with the presence of a strong cellular proliferative response to the immunizing shOSP protein. Analysis of the cellular responses in combination with neuropathological observations also indicates an important role for neutrophils in the disease process. Interestingly, all immunized monkeys developed antibody responses to OSP peptide 103-123, a B cell epitope previously identified in MS patients. These responses did not correlate with the development of clinical disease, but may have relevance as a biomarker for immunoreactivity towards OSP in myelin disorders. Our data demonstrate that in rhesus monkeys immune responses directed at OSP are encephalitogenic, leading to inflammatory responses throughout the central nervous system and to selective demyelination of the optic nerve.

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Osp/Claudin-11 Forms a Complex with a Novel Member of the Tetraspanin Super Family and β1 Integrin and Regulates Proliferation and Migration of Oligodendrocytes

Cited by 173 publications

References 65 publications

Claudin-2 is selectively enriched in and promotes the formation of breast cancer liver metastases through engagement of integrin complexes

Claudin-2 is selectively enriched in and promotes the formation of breast cancer liver metastases through engagement of integrin complexes

Expression of Transcripts for Myelin Related Genes in Postmortem Brain from Cocaine Abusers

Oligodendrocyte‐specific protein is encephalitogenic in rhesus macaques and induces specific demyelination of the optic nerve

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