Oxalate stimulates IL-6 production in HK-2 cells, a line of human renal proximal tubular epithelial cells
Oxalate stimulates IL-6 production in HK-2 cells, a line of human renal proximal tubular epithelial cells. Oxalate is a metabolic end product excreted primarily by the kidney and associated with several pathologic conditions. The most common pathologic condition involving oxalate is the formation of...
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| description | Oxalate stimulates IL-6 production in HK-2 cells, a line of human renal proximal tubular epithelial cells.
Oxalate is a metabolic end product excreted primarily by the kidney and associated with several pathologic conditions. The most common pathologic condition involving oxalate is the formation of calcium oxalate stones in the kidney. Several stimuli have been implicated in the development of glomerular and tubular injury in various forms of immune-mediated renal diseases. The elevated level of interleukin-6 (IL-6) has been reported in the urine of kidney stone-forming patients. In the present study, we investigated the role of oxalate, a major constituent of calcium oxalate kidney stone disease, in the production of IL-6 in normal human HK-2 kidney cells.
Confluent cultures of HK-2 cells (a renal epithelial cell line of human origin) were exposed to various concentrations of oxalate (0.2 to 2.0mmol/L) and lipopolysaccharide (LPS) (0.1 and 10 μg/mL) for various time points (4-24 h) under serum-free conditions. The conditioned mediums were collected, and an IL-6 protein level was measured by enzyme-linked immunosorbent assay (ELISA). The total cellular RNA was isolated from the cells and subjected to relative quantitative reverse transcription-polymerase chain reaction (RT-PCR) to determine the expression of IL-6 mRNA. The statistical analysis of the results was carried out using the Student t test.
HK-2 cells express IL-6 mRNA and protein. Oxalate increased the secretion of IL-6 protein in HK-2 cells in a concentration-dependent fashion. Oxalate exposure to HK-2 cells also induced transcriptional up-regulation of the IL-6 gene, as determined by the increased level of IL-6 mRNA expression following treatment with oxalate. Moreover, the effects of oxalate on IL-6 expression were time- and concentration-dependent. This is the first report demonstrating the regulation of IL-6 by oxalate.
This study provides the first direct evidence that oxalate up-regulates the expression and secretion of IL-6 in renal epithelial cells. The increased IL-6 expression and secretion by renal epithelial cells may play a critical role in the progression of urolithiasis in hyperoxaluric conditions. |
| doi_str_mv | 10.1111/j.1523-1755.2005.00427.x |
| format | Article |
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Oxalate is a metabolic end product excreted primarily by the kidney and associated with several pathologic conditions. The most common pathologic condition involving oxalate is the formation of calcium oxalate stones in the kidney. Several stimuli have been implicated in the development of glomerular and tubular injury in various forms of immune-mediated renal diseases. The elevated level of interleukin-6 (IL-6) has been reported in the urine of kidney stone-forming patients. In the present study, we investigated the role of oxalate, a major constituent of calcium oxalate kidney stone disease, in the production of IL-6 in normal human HK-2 kidney cells.
Confluent cultures of HK-2 cells (a renal epithelial cell line of human origin) were exposed to various concentrations of oxalate (0.2 to 2.0mmol/L) and lipopolysaccharide (LPS) (0.1 and 10 μg/mL) for various time points (4-24 h) under serum-free conditions. The conditioned mediums were collected, and an IL-6 protein level was measured by enzyme-linked immunosorbent assay (ELISA). The total cellular RNA was isolated from the cells and subjected to relative quantitative reverse transcription-polymerase chain reaction (RT-PCR) to determine the expression of IL-6 mRNA. The statistical analysis of the results was carried out using the Student t test.
HK-2 cells express IL-6 mRNA and protein. Oxalate increased the secretion of IL-6 protein in HK-2 cells in a concentration-dependent fashion. Oxalate exposure to HK-2 cells also induced transcriptional up-regulation of the IL-6 gene, as determined by the increased level of IL-6 mRNA expression following treatment with oxalate. Moreover, the effects of oxalate on IL-6 expression were time- and concentration-dependent. This is the first report demonstrating the regulation of IL-6 by oxalate.
This study provides the first direct evidence that oxalate up-regulates the expression and secretion of IL-6 in renal epithelial cells. The increased IL-6 expression and secretion by renal epithelial cells may play a critical role in the progression of urolithiasis in hyperoxaluric conditions.</description><identifier>ISSN: 0085-2538</identifier><identifier>EISSN: 1523-1755</identifier><identifier>DOI: 10.1111/j.1523-1755.2005.00427.x</identifier><identifier>PMID: 16014026</identifier><identifier>CODEN: KDYIA5</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Biological and medical sciences ; Cell Line ; Dose-Response Relationship, Drug ; Errors of metabolism ; Gene Expression - drug effects ; Humans ; hyperoxaluria ; Hyperoxaluria - physiopathology ; interleukin-6 ; Interleukin-6 - genetics ; Interleukin-6 - metabolism ; Interleukin-6 - secretion ; Kidney Tubules, Proximal - cytology ; Kidney Tubules, Proximal - drug effects ; Kidney Tubules, Proximal - physiology ; Lipopolysaccharides - pharmacology ; Medical sciences ; Metabolic diseases ; Miscellaneous hereditary metabolic disorders ; Nephrology. Urinary tract diseases ; Oxalates - pharmacology ; proinflammatory cytokines ; RNA, Messenger - analysis ; Up-Regulation - drug effects ; Urinary Calculi - physiopathology ; Urinary lithiasis ; urolithiasis</subject><ispartof>Kidney international, 2005-08, Vol.68 (2), p.497-503</ispartof><rights>2005 International Society of Nephrology</rights><rights>2005 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Aug 2005</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c567t-c9d5eea9098fae787f08779cffc1a0794ae55544b4c182941ff1e8ebbce9189f3</citedby><cites>FETCH-LOGICAL-c567t-c9d5eea9098fae787f08779cffc1a0794ae55544b4c182941ff1e8ebbce9189f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.proquest.com/docview/210168368?pq-origsite=primo$$EHTML$$P50$$Gproquest$$H</linktohtml><link.rule.ids>314,780,784,27923,27924,64384,64386,64388,72240</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17008589$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16014026$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Huang, Mei Yi</creatorcontrib><creatorcontrib>Chaturvedi, Lakshmi S.</creatorcontrib><creatorcontrib>Koul, Sweaty</creatorcontrib><creatorcontrib>Koul, Hari K.</creatorcontrib><title>Oxalate stimulates IL-6 production in HK-2 cells, a line of human renal proximal tubular epithelial cells</title><title>Kidney international</title><addtitle>Kidney Int</addtitle><description>Oxalate stimulates IL-6 production in HK-2 cells, a line of human renal proximal tubular epithelial cells.
Oxalate is a metabolic end product excreted primarily by the kidney and associated with several pathologic conditions. The most common pathologic condition involving oxalate is the formation of calcium oxalate stones in the kidney. Several stimuli have been implicated in the development of glomerular and tubular injury in various forms of immune-mediated renal diseases. The elevated level of interleukin-6 (IL-6) has been reported in the urine of kidney stone-forming patients. In the present study, we investigated the role of oxalate, a major constituent of calcium oxalate kidney stone disease, in the production of IL-6 in normal human HK-2 kidney cells.
Confluent cultures of HK-2 cells (a renal epithelial cell line of human origin) were exposed to various concentrations of oxalate (0.2 to 2.0mmol/L) and lipopolysaccharide (LPS) (0.1 and 10 μg/mL) for various time points (4-24 h) under serum-free conditions. The conditioned mediums were collected, and an IL-6 protein level was measured by enzyme-linked immunosorbent assay (ELISA). The total cellular RNA was isolated from the cells and subjected to relative quantitative reverse transcription-polymerase chain reaction (RT-PCR) to determine the expression of IL-6 mRNA. The statistical analysis of the results was carried out using the Student t test.
HK-2 cells express IL-6 mRNA and protein. Oxalate increased the secretion of IL-6 protein in HK-2 cells in a concentration-dependent fashion. Oxalate exposure to HK-2 cells also induced transcriptional up-regulation of the IL-6 gene, as determined by the increased level of IL-6 mRNA expression following treatment with oxalate. Moreover, the effects of oxalate on IL-6 expression were time- and concentration-dependent. This is the first report demonstrating the regulation of IL-6 by oxalate.
This study provides the first direct evidence that oxalate up-regulates the expression and secretion of IL-6 in renal epithelial cells. The increased IL-6 expression and secretion by renal epithelial cells may play a critical role in the progression of urolithiasis in hyperoxaluric conditions.</description><subject>Biological and medical sciences</subject><subject>Cell Line</subject><subject>Dose-Response Relationship, Drug</subject><subject>Errors of metabolism</subject><subject>Gene Expression - drug effects</subject><subject>Humans</subject><subject>hyperoxaluria</subject><subject>Hyperoxaluria - physiopathology</subject><subject>interleukin-6</subject><subject>Interleukin-6 - genetics</subject><subject>Interleukin-6 - metabolism</subject><subject>Interleukin-6 - secretion</subject><subject>Kidney Tubules, Proximal - cytology</subject><subject>Kidney Tubules, Proximal - drug effects</subject><subject>Kidney Tubules, Proximal - physiology</subject><subject>Lipopolysaccharides - pharmacology</subject><subject>Medical sciences</subject><subject>Metabolic diseases</subject><subject>Miscellaneous hereditary metabolic disorders</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Oxalates - pharmacology</subject><subject>proinflammatory cytokines</subject><subject>RNA, Messenger - analysis</subject><subject>Up-Regulation - drug effects</subject><subject>Urinary Calculi - physiopathology</subject><subject>Urinary lithiasis</subject><subject>urolithiasis</subject><issn>0085-2538</issn><issn>1523-1755</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNqFkU2PFCEQhonRuOPoT9AQE_dkt0BDA0fdrO7GSfaiZ0LTRZZJf4zQmPHfS-9MdhMvEhIK6qlK8b4IYUpqWtanfU0FayoqhagZIaImhDNZH5-hzWPiOdoQokTFRKMu0KuU9qTcdUNeogvaEsoJazco3B3tYBfAaQljXqOEb3dViw9x7rNbwjzhMOGb7xXDDoYhfcQWD2ECPHt8n0c74QiTHVb-GMYSLLkrfSKGQ1juYQjl6aHwNXrh7ZDgzfncop9fr39c3VS7u2-3V593lROtXCqnewFgNdHKW5BKeqKk1M57Ry2RmlsQQnDecUcV05x6T0FB1znQVGnfbNHlqW-Z6FeGtJgxpHUCO8Gck2kVYVq2vIDv_wH3c47lL8kwSmirmrK3SJ0gF-eUInhziOWb8Y-hxKxemL1ZJTer5Gb1wjx4YY6l9N25f-5G6J8Kz-IX4MMZsMnZwUc7uZCeOLn6VxzborcnbrJLjvAIcK5bykjJfznlocj6O0A0yQWYHPQhgltMP4f_T_sXz66xDw</recordid><startdate>20050801</startdate><enddate>20050801</enddate><creator>Huang, Mei Yi</creator><creator>Chaturvedi, Lakshmi S.</creator><creator>Koul, Sweaty</creator><creator>Koul, Hari K.</creator><general>Elsevier Inc</general><general>Nature Publishing</general><general>Elsevier Limited</general><scope>6I.</scope><scope>AAFTH</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QP</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20050801</creationdate><title>Oxalate stimulates IL-6 production in HK-2 cells, a line of human renal proximal tubular epithelial cells</title><author>Huang, Mei Yi ; Chaturvedi, Lakshmi S. ; Koul, Sweaty ; Koul, Hari K.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c567t-c9d5eea9098fae787f08779cffc1a0794ae55544b4c182941ff1e8ebbce9189f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Biological and medical sciences</topic><topic>Cell Line</topic><topic>Dose-Response Relationship, Drug</topic><topic>Errors of metabolism</topic><topic>Gene Expression - drug effects</topic><topic>Humans</topic><topic>hyperoxaluria</topic><topic>Hyperoxaluria - physiopathology</topic><topic>interleukin-6</topic><topic>Interleukin-6 - genetics</topic><topic>Interleukin-6 - metabolism</topic><topic>Interleukin-6 - secretion</topic><topic>Kidney Tubules, Proximal - cytology</topic><topic>Kidney Tubules, Proximal - drug effects</topic><topic>Kidney Tubules, Proximal - physiology</topic><topic>Lipopolysaccharides - pharmacology</topic><topic>Medical sciences</topic><topic>Metabolic diseases</topic><topic>Miscellaneous hereditary metabolic disorders</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Oxalates - pharmacology</topic><topic>proinflammatory cytokines</topic><topic>RNA, Messenger - analysis</topic><topic>Up-Regulation - drug effects</topic><topic>Urinary Calculi - physiopathology</topic><topic>Urinary lithiasis</topic><topic>urolithiasis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Huang, Mei Yi</creatorcontrib><creatorcontrib>Chaturvedi, Lakshmi S.</creatorcontrib><creatorcontrib>Koul, Sweaty</creatorcontrib><creatorcontrib>Koul, Hari K.</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Kidney international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Huang, Mei Yi</au><au>Chaturvedi, Lakshmi S.</au><au>Koul, Sweaty</au><au>Koul, Hari K.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Oxalate stimulates IL-6 production in HK-2 cells, a line of human renal proximal tubular epithelial cells</atitle><jtitle>Kidney international</jtitle><addtitle>Kidney Int</addtitle><date>2005-08-01</date><risdate>2005</risdate><volume>68</volume><issue>2</issue><spage>497</spage><epage>503</epage><pages>497-503</pages><issn>0085-2538</issn><eissn>1523-1755</eissn><coden>KDYIA5</coden><abstract>Oxalate stimulates IL-6 production in HK-2 cells, a line of human renal proximal tubular epithelial cells.
Oxalate is a metabolic end product excreted primarily by the kidney and associated with several pathologic conditions. The most common pathologic condition involving oxalate is the formation of calcium oxalate stones in the kidney. Several stimuli have been implicated in the development of glomerular and tubular injury in various forms of immune-mediated renal diseases. The elevated level of interleukin-6 (IL-6) has been reported in the urine of kidney stone-forming patients. In the present study, we investigated the role of oxalate, a major constituent of calcium oxalate kidney stone disease, in the production of IL-6 in normal human HK-2 kidney cells.
Confluent cultures of HK-2 cells (a renal epithelial cell line of human origin) were exposed to various concentrations of oxalate (0.2 to 2.0mmol/L) and lipopolysaccharide (LPS) (0.1 and 10 μg/mL) for various time points (4-24 h) under serum-free conditions. The conditioned mediums were collected, and an IL-6 protein level was measured by enzyme-linked immunosorbent assay (ELISA). The total cellular RNA was isolated from the cells and subjected to relative quantitative reverse transcription-polymerase chain reaction (RT-PCR) to determine the expression of IL-6 mRNA. The statistical analysis of the results was carried out using the Student t test.
HK-2 cells express IL-6 mRNA and protein. Oxalate increased the secretion of IL-6 protein in HK-2 cells in a concentration-dependent fashion. Oxalate exposure to HK-2 cells also induced transcriptional up-regulation of the IL-6 gene, as determined by the increased level of IL-6 mRNA expression following treatment with oxalate. Moreover, the effects of oxalate on IL-6 expression were time- and concentration-dependent. This is the first report demonstrating the regulation of IL-6 by oxalate.
This study provides the first direct evidence that oxalate up-regulates the expression and secretion of IL-6 in renal epithelial cells. The increased IL-6 expression and secretion by renal epithelial cells may play a critical role in the progression of urolithiasis in hyperoxaluric conditions.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>16014026</pmid><doi>10.1111/j.1523-1755.2005.00427.x</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Biological and medical sciences Cell Line Dose-Response Relationship, Drug Errors of metabolism Gene Expression - drug effects Humans hyperoxaluria Hyperoxaluria - physiopathology interleukin-6 Interleukin-6 - genetics Interleukin-6 - metabolism Interleukin-6 - secretion Kidney Tubules, Proximal - cytology Kidney Tubules, Proximal - drug effects Kidney Tubules, Proximal - physiology Lipopolysaccharides - pharmacology Medical sciences Metabolic diseases Miscellaneous hereditary metabolic disorders Nephrology. Urinary tract diseases Oxalates - pharmacology proinflammatory cytokines RNA, Messenger - analysis Up-Regulation - drug effects Urinary Calculi - physiopathology Urinary lithiasis urolithiasis |
| title | Oxalate stimulates IL-6 production in HK-2 cells, a line of human renal proximal tubular epithelial cells |
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