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"https://www.academia.edu/login?post_login_redirect_url=https%3A%2F%2Fwww.academia.edu%2F17906349%2FHypoxia_induced_matrix_metalloproteinase_13_expression_in_astrocytes_enhances_permeability_of_brain_endothelial_cells%3Fshow_translation%3Dtrue"; window.loswp.previewableAttachments = [{"id":39773304,"identifier":"Attachment_39773304","shouldShowBulkDownload":false}]; window.loswp.shouldDetectTimezone = true; window.loswp.shouldShowBulkDownload = true; window.loswp.showSignupCaptcha = false window.loswp.willEdgeCache = false; window.loswp.work = {"work":{"id":17906349,"created_at":"2015-11-07T06:50:11.184-08:00","from_world_paper_id":143956382,"updated_at":"2024-11-17T10:30:45.215-08:00","_data":{"grobid_abstract":"Matrix metalloproteinase-13 (MMP-13) is involved in the degradation of extracellular matrix in many kinds of tissues. Here we found that hypoxia increased MMP-13 protein and mRNA levels in primary rat astrocyte cultures. Hypoxia stimulation also increased the secretion of MMP-13 from astrocytes, as shown by zymographic analysis. In addition, exposure to hypoxia up-regulated the expression of c-Fos and c-Jun time-dependently. Hypoxia-induced MMP-13 overexpression was antagonized by transfection with antisense oligodeoxynucleotides (AS-ODN) of c-Fos or c-Jun. Furthermore, hypoxic-conditioned medium (Hx-CM) collected from astrocytes exposed to hypoxia increased paracellular permeability of adult rat brain endothelial cells (ARBECs). Administration of MMP-13 neutralizing antibody antagonized Hx-CM-induced paracellular permeability of ARBECs. Furthermore, pre-transfection of astrocytes with AS-ODN of c-Fos, c-Jun or MMP-13-shRNA significantly decreased hyperpermeability of ARBECs induced by Hx-CM. The arrangement of tight junction protein (TJP) zonular occludens-1 (ZO-1) of ARBECs disorganized in response to Hx-CM. Administration of Hx-CM to ARBECs also resulted in the production of proteolytic fragments of ZO-1, which was antagonized by transfection of MMP-13-shRNA in primary astrocytes. Administration of MMP-13 recombinant protein to ARBECs led to the disorganization and fragmentation of ZO-1 protein and also increased paracellular permeability. These results suggest that hypoxia-induced MMP-13 expression in astrocytes is regulated by c-Fos and c-Jun. MMP-13 is an important factor leading to the disorganization of ZO-1 and hyperpermeablility of blood-brain barrier in response to hypoxia.","publication_date":"2009,,","publication_name":"Journal of Cellular Physiology","grobid_abstract_attachment_id":"39773304"},"document_type":"paper","pre_hit_view_count_baseline":null,"quality":"high","language":"en","title":"Hypoxia-induced matrix metalloproteinase-13 expression in astrocytes enhances permeability of brain endothelial cells","broadcastable":false,"draft":null,"has_indexable_attachment":true,"indexable":true}}["work"]; window.loswp.workCoauthors = [37822776]; window.loswp.locale = "en"; window.loswp.countryCode = "SG"; window.loswp.cwvAbTestBucket = ""; window.loswp.designVariant = "ds_vanilla"; window.loswp.fullPageMobileSutdModalVariant = "control"; window.loswp.useOptimizedScribd4genScript = false; window.loswp.appleClientId = 'edu.academia.applesignon';</script><script defer="" 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data-author-id="64034623" href="https://independent.academia.edu/JasonHuber5">Jason Huber</a></div><p class="ds-related-work--metadata ds2-5-body-xs">Journal of Cell Science, 2003</p><p class="ds-related-work--abstract ds2-5-body-sm">Co-culture with glial cells and glia-conditioned media can induce blood-brain barrier properties in microvessel endothelial cells and protect against hypoxia-induced blood-brain barrier breakdown. We examined the effect of two types of glia-conditioned media on brain microvessel endothelial cell permeability and tight junction protein expression, and studied potential mechanisms of action. We found that C6-glioma-conditioned media, but not rat astrocyte-conditioned media, protected against an increase in permeability induced by exposure to 1% oxygen for 24 hours. This hypoxic stress caused an increase in the expression of tight junction proteins claudin-1 and actin,particularly in cells treated with C6-conditioned media. We found that C6-conditioned media has a significantly higher level of both basic fibroblast growth factor and vascular endothelial growth factor. Treatment with C6-conditioned media for 1 or 3 days protects against hypoxia-induced permeability increases, and this p...</p><div class="ds-related-work--ctas"><button class="ds2-5-text-link ds2-5-text-link--inline js-swp-download-button" data-signup-modal="{"location":"wsj-grid-card-download-pdf-modal","work_title":"Protection against hypoxia-induced increase in blood-brain barrier permeability: role of tight junction proteins and NFkappaB","attachmentId":75049352,"attachmentType":"pdf","work_url":"https://www.academia.edu/62215242/Protection_against_hypoxia_induced_increase_in_blood_brain_barrier_permeability_role_of_tight_junction_proteins_and_NFkappaB","alternativeTracking":true}"><span class="material-symbols-outlined" style="font-size: 18px" translate="no">download</span><span class="ds2-5-text-link__content">Download free PDF</span></button><a class="ds2-5-text-link ds2-5-text-link--inline js-wsj-grid-card-view-pdf" href="https://www.academia.edu/62215242/Protection_against_hypoxia_induced_increase_in_blood_brain_barrier_permeability_role_of_tight_junction_proteins_and_NFkappaB"><span class="ds2-5-text-link__content">View PDF</span><span class="material-symbols-outlined" style="font-size: 18px" translate="no">chevron_right</span></a></div></div><div class="ds-related-work--container js-wsj-grid-card" data-collection-position="4" data-entity-id="98172530" data-sort-order="default"><a class="ds-related-work--title js-wsj-grid-card-title ds2-5-body-md ds2-5-body-link" href="https://www.academia.edu/98172530/Effects_of_hypoxia_reoxygenation_on_rat_blood_brain_barrier_permeability_and_tight_junctional_protein_expression">Effects of hypoxia-reoxygenation on rat blood-brain barrier permeability and tight junctional protein expression</a><div class="ds-related-work--metadata"><a class="js-wsj-grid-card-author ds2-5-body-sm ds2-5-body-link" data-author-id="38289730" href="https://independent.academia.edu/ThomasDavis24">Thomas Davis</a></div><p class="ds-related-work--metadata ds2-5-body-xs">American journal of physiology. Heart and circulatory physiology, 2003</p><p class="ds-related-work--abstract ds2-5-body-sm">Cerebral microvessel endothelial cells that form the blood-brain barrier (BBB) have tight junctions (TJs) that are critical for maintaining brain homeostasis. The effects of initial reoxygenation after a hypoxic insult (H/R) on functional and molecular properties of the BBB and TJs remain unclear. In situ brain perfusion and Western blot analyses were performed to assess in vivo BBB integrity on reoxygenation after a hypoxic insult of 6% O2 for 1 h. Model conditions [blood pressure, blood gas chemistries, cerebral blood flow (CBF), and brain ATP concentration] were also assessed to ensure consistent levels and criteria for insult. In situ brain perfusion revealed that initial reoxygenation (10 min) significantly increased the uptake of [14C]sucrose into brain parenchyma. Capillary depletion and CBF analyses indicated the perturbations were due to increased paracellular permeability rather than vascular volume changes. Hypoxia with reoxygenation (10 min) produced an increase in BBB p...</p><div class="ds-related-work--ctas"><button class="ds2-5-text-link ds2-5-text-link--inline js-swp-download-button" data-signup-modal="{"location":"wsj-grid-card-download-pdf-modal","work_title":"Effects of hypoxia-reoxygenation on rat blood-brain barrier permeability and tight junctional protein expression","attachmentId":99596408,"attachmentType":"pdf","work_url":"https://www.academia.edu/98172530/Effects_of_hypoxia_reoxygenation_on_rat_blood_brain_barrier_permeability_and_tight_junctional_protein_expression","alternativeTracking":true}"><span class="material-symbols-outlined" style="font-size: 18px" translate="no">download</span><span class="ds2-5-text-link__content">Download free PDF</span></button><a class="ds2-5-text-link ds2-5-text-link--inline js-wsj-grid-card-view-pdf" href="https://www.academia.edu/98172530/Effects_of_hypoxia_reoxygenation_on_rat_blood_brain_barrier_permeability_and_tight_junctional_protein_expression"><span class="ds2-5-text-link__content">View PDF</span><span class="material-symbols-outlined" style="font-size: 18px" translate="no">chevron_right</span></a></div></div><div class="ds-related-work--container js-wsj-grid-card" data-collection-position="5" data-entity-id="25201954" data-sort-order="default"><a class="ds-related-work--title js-wsj-grid-card-title ds2-5-body-md ds2-5-body-link" href="https://www.academia.edu/25201954/Connexin43_phosphorylation_state_and_intercellular_communication_in_cultured_astrocytes_following_hypoxia_and_protein_phosphatase_inhibition">Connexin43 phosphorylation state and intercellular communication in cultured astrocytes following hypoxia and protein phosphatase inhibition</a><div class="ds-related-work--metadata"><a class="js-wsj-grid-card-author ds2-5-body-sm ds2-5-body-link" data-author-id="41763670" href="https://umanitoba.academia.edu/JNagy">James I Nagy</a></div><p class="ds-related-work--abstract ds2-5-body-sm">The effects of hypoxia and phosphatase inhibitors on connexin43 (Cx43) phosphorylation state, gap junctional intercellular communication (GJIC) and immunolabelling with anti-Cx43 antibodies were investigated in cultured astrocytes. Astrocytes contained predominantly phosphorylated forms of Cx43 and these underwent dephosphorylation 30 min after hypoxia. This was preceded by a 77% reduction in GJIC 15 min after hypoxia, indicating that reduced GJIC occurs prior to Cx43 dephosphorylation. Hypoxia caused a reduction in punctate immunostaining (epitope masking) at cell-cell contacts with one anti-Cx43 antibody, and increased labelling with another antibody (13-8300) that detects only a dephosphorylated form of Cx43. Inhibition of protein phosphatase (PP)-1 and PP-2A with okadaic acid or calyculin A had little effect on hypoxia-induced Cx43 dephosphorylation. Inhibition of PP-2B (calcineurin) with cyclosporin A or FK506 reduced Cx43 dephosphorylation and junctional uncoupling seen after hypoxia. These results demonstrate that responses of astrocytic Cx43 to hypoxia in vitro are similar to those seen after ischaemia in vivo, and that inhibition of protein phosphatase protects astrocytes from hypoxia-induced Cx43 dephosphorylation and junctional uncoupling. In addition, calcineurin may play a direct role in the regulation of astrocytic GJIC and Cx43 phosphorylation state.</p><div class="ds-related-work--ctas"><button class="ds2-5-text-link ds2-5-text-link--inline js-swp-download-button" data-signup-modal="{"location":"wsj-grid-card-download-pdf-modal","work_title":"Connexin43 phosphorylation state and intercellular communication in cultured astrocytes following hypoxia and protein phosphatase inhibition","attachmentId":45548482,"attachmentType":"pdf","work_url":"https://www.academia.edu/25201954/Connexin43_phosphorylation_state_and_intercellular_communication_in_cultured_astrocytes_following_hypoxia_and_protein_phosphatase_inhibition","alternativeTracking":true}"><span class="material-symbols-outlined" style="font-size: 18px" translate="no">download</span><span class="ds2-5-text-link__content">Download free PDF</span></button><a class="ds2-5-text-link ds2-5-text-link--inline js-wsj-grid-card-view-pdf" href="https://www.academia.edu/25201954/Connexin43_phosphorylation_state_and_intercellular_communication_in_cultured_astrocytes_following_hypoxia_and_protein_phosphatase_inhibition"><span class="ds2-5-text-link__content">View PDF</span><span class="material-symbols-outlined" style="font-size: 18px" translate="no">chevron_right</span></a></div></div><div class="ds-related-work--container js-wsj-grid-card" data-collection-position="6" data-entity-id="121633964" data-sort-order="default"><a class="ds-related-work--title js-wsj-grid-card-title ds2-5-body-md ds2-5-body-link" href="https://www.academia.edu/121633964/Impact_of_Hypoxia_on_Astrocyte_Induced_Pathogenesis">Impact of Hypoxia on Astrocyte Induced Pathogenesis</a><div class="ds-related-work--metadata"><a class="js-wsj-grid-card-author ds2-5-body-sm ds2-5-body-link" data-author-id="298030027" href="https://independent.academia.edu/NIDAALFIANACHOIRPENDIDIKANAGAMAISLAM">NIDA ALFIANA CHOIR PENDIDIKAN AGAMA ISLAM</a></div><p class="ds-related-work--metadata ds2-5-body-xs">Astrocytes in Brain Communication and Disease [Working Title]</p><p class="ds-related-work--abstract ds2-5-body-sm">Astrocytes are the most abundant cells of the central nervous system. These cells are of diverse types based on their function and structure. Astrocyte activation is linked mainly with microbial infections, but long-term activation can lead to neurological impairment. Astrocytes play a significant role in neuro-inflammation by activating pro-inflammatory pathways. Activation of interleukins and cytokines causes neuroinflammation resulting in many neurodegenerative disorders such as stroke, growth of tumours, and Alzheimer’s. Inflammation of the brain hinders neural circulation and compromises blood flow by affecting the blood–brain barrier. So the oxygen concentration is lowered, causing brain hypoxia. Hypoxia leads to the activation of nuclear factor kappa B (NFkB) and hypoxia-inducible factors (HIF), which aggravates the inflammatory state of the brain. Hypoxia evoked changes in the blood–brain barrier, further complicating astrocyte-induced pathogenesis.</p><div class="ds-related-work--ctas"><button class="ds2-5-text-link ds2-5-text-link--inline js-swp-download-button" data-signup-modal="{"location":"wsj-grid-card-download-pdf-modal","work_title":"Impact of Hypoxia on Astrocyte Induced Pathogenesis","attachmentId":116465288,"attachmentType":"pdf","work_url":"https://www.academia.edu/121633964/Impact_of_Hypoxia_on_Astrocyte_Induced_Pathogenesis","alternativeTracking":true}"><span class="material-symbols-outlined" style="font-size: 18px" translate="no">download</span><span class="ds2-5-text-link__content">Download free PDF</span></button><a class="ds2-5-text-link ds2-5-text-link--inline js-wsj-grid-card-view-pdf" href="https://www.academia.edu/121633964/Impact_of_Hypoxia_on_Astrocyte_Induced_Pathogenesis"><span class="ds2-5-text-link__content">View PDF</span><span class="material-symbols-outlined" style="font-size: 18px" 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data-sort-order="default"><a class="ds-related-work--title js-related-work-grid-card-title ds2-5-body-md ds2-5-body-link" href="https://www.academia.edu/81691697/Hypoxia_independent_mechanisms_of_HIF_1%CE%B1_expression_in_astrocytes_after_ischemic_preconditioning">Hypoxia-independent mechanisms of HIF-1α expression in astrocytes after ischemic preconditioning</a><div class="ds-related-work--metadata"><a class="js-related-work-grid-card-author ds2-5-body-sm ds2-5-body-link" data-author-id="32797713" href="https://independent.academia.edu/SchuichiKoizumi">Schuichi Koizumi</a></div><p class="ds-related-work--metadata ds2-5-body-xs">Glia, 2017</p><div class="ds-related-work--ctas"><button class="ds2-5-text-link ds2-5-text-link--inline js-swp-download-button" data-signup-modal="{"location":"wsj-grid-card-download-pdf-modal","work_title":"Hypoxia-independent mechanisms of HIF-1α expression in astrocytes after ischemic 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class="js-related-work-grid-card-author ds2-5-body-sm ds2-5-body-link" data-author-id="180204303" href="https://cambridge.academia.edu/StephenHladky">Stephen Hladky</a></div><p class="ds-related-work--metadata ds2-5-body-xs">Journal of Neurochemistry, 2009</p><div class="ds-related-work--ctas"><button class="ds2-5-text-link ds2-5-text-link--inline js-swp-download-button" data-signup-modal="{"location":"wsj-grid-card-download-pdf-modal","work_title":"P-glycoprotein expression in immortalised rat brain endothelial cells: comparisons following exogenously applied hydrogen peroxide and after hypoxia-reoxygenation","attachmentId":65069944,"attachmentType":"pdf","work_url":"https://www.academia.edu/44606144/P_glycoprotein_expression_in_immortalised_rat_brain_endothelial_cells_comparisons_following_exogenously_applied_hydrogen_peroxide_and_after_hypoxia_reoxygenation","alternativeTracking":true}"><span class="material-symbols-outlined" style="font-size: 18px" 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