Thyrocytes Isolated from Autoimmune-Diseased Thyroids Secrete Soluble Tumor Necrosis Factor-R1 That Is Related to Their Elevated Protein Kinase C Activity
Soluble tumor necrosis factor (TNF)-α receptors have the potential to modulate TNF-α activity during autoimmune thyroiditis. In this study we examined cell-surface TNF-α receptors and soluble TNF-α receptor production by thyrocytes from normal and MRL-lpr -/- (diseased) mice, which spontaneously dev...
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| Veröffentlicht in: | Thyroid (New York, N.Y.) N.Y.), 2004-04, Vol.14 (4), p.249-262 |
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| creator | LaBue, M. Colburn, K.K. Green, L.M. |
| description | Soluble tumor necrosis factor (TNF)-α receptors have the potential to modulate TNF-α activity during autoimmune thyroiditis. In this study we examined cell-surface TNF-α receptors and
soluble TNF-α receptor production by thyrocytes from normal and MRL-lpr
-/-
(diseased) mice, which spontaneously develop autoimmune thyroiditis. We found that murine thyrocytes possess the 55-kd receptor
(TNF-R1). Examination of soluble TNF-R1 production revealed that diseased thyrocytes produced sevenfold more soluble TNF-R1 than normal thyrocytes. Furthermore, basal protein kinase C (pKC) activity in
diseased thyrocytes was 67% higher than that found in normal murine thyrocytes. The elevated basal pKC activity in diseased thyrocytes was related to their enhanced production of soluble TNF-R1 because
inhibition of pKC activity with calphostin C caused soluble TNF-R1 production to decrease significantly. Additionally, soluble TNF-R1 production by murine thyrocytes was not a result of cell-surface receptor
shedding but through secretion of a truncated version of TNF-R1. This was evident when cell-surface TNF-R1 levels were unchanged after treatment of diseased thyrocytes with calphostin C. Also, the 28-kd
form of TNF-R1, which corresponds to the soluble receptor, was present in the intracellular membranes of the diseased thyrocytes. |
| doi_str_mv | 10.1089/105072504323030906 |
| format | Article |
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soluble TNF-α receptor production by thyrocytes from normal and MRL-lpr
-/-
(diseased) mice, which spontaneously develop autoimmune thyroiditis. We found that murine thyrocytes possess the 55-kd receptor
(TNF-R1). Examination of soluble TNF-R1 production revealed that diseased thyrocytes produced sevenfold more soluble TNF-R1 than normal thyrocytes. Furthermore, basal protein kinase C (pKC) activity in
diseased thyrocytes was 67% higher than that found in normal murine thyrocytes. The elevated basal pKC activity in diseased thyrocytes was related to their enhanced production of soluble TNF-R1 because
inhibition of pKC activity with calphostin C caused soluble TNF-R1 production to decrease significantly. Additionally, soluble TNF-R1 production by murine thyrocytes was not a result of cell-surface receptor
shedding but through secretion of a truncated version of TNF-R1. This was evident when cell-surface TNF-R1 levels were unchanged after treatment of diseased thyrocytes with calphostin C. Also, the 28-kd
form of TNF-R1, which corresponds to the soluble receptor, was present in the intracellular membranes of the diseased thyrocytes.</description><identifier>ISSN: 1050-7256</identifier><identifier>EISSN: 1557-9077</identifier><identifier>DOI: 10.1089/105072504323030906</identifier><identifier>PMID: 15142358</identifier><language>eng</language><publisher>United States: Mary Ann Liebert, Inc</publisher><subject>Animals ; Cells, Cultured ; Disease Models, Animal ; Laboratory Research Reports ; Mice ; Mice, Inbred MRL lpr ; Mice, Knockout ; Protein Kinase C - metabolism ; Receptors, Tumor Necrosis Factor, Type I - biosynthesis ; Receptors, Tumor Necrosis Factor, Type I - physiology ; Reference Values ; Space life sciences ; Thyroid Gland - pathology ; Thyroid Gland - physiology ; Thyroiditis, Autoimmune - enzymology ; Thyroiditis, Autoimmune - physiopathology</subject><ispartof>Thyroid (New York, N.Y.), 2004-04, Vol.14 (4), p.249-262</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c299t-3a5747037010cd781132ffa6673ccada915ab8b6552e83491c79e4f198e2b5ed3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.liebertpub.com/doi/epdf/10.1089/105072504323030906$$EPDF$$P50$$Gmaryannliebert$$H</linktopdf><linktohtml>$$Uhttps://www.liebertpub.com/doi/full/10.1089/105072504323030906$$EHTML$$P50$$Gmaryannliebert$$H</linktohtml><link.rule.ids>314,776,780,3029,21702,27901,27902,55266,55278</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15142358$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>LaBue, M.</creatorcontrib><creatorcontrib>Colburn, K.K.</creatorcontrib><creatorcontrib>Green, L.M.</creatorcontrib><title>Thyrocytes Isolated from Autoimmune-Diseased Thyroids Secrete Soluble Tumor Necrosis Factor-R1 That Is Related to Their Elevated Protein Kinase C Activity</title><title>Thyroid (New York, N.Y.)</title><addtitle>Thyroid</addtitle><description>Soluble tumor necrosis factor (TNF)-α receptors have the potential to modulate TNF-α activity during autoimmune thyroiditis. In this study we examined cell-surface TNF-α receptors and
soluble TNF-α receptor production by thyrocytes from normal and MRL-lpr
-/-
(diseased) mice, which spontaneously develop autoimmune thyroiditis. We found that murine thyrocytes possess the 55-kd receptor
(TNF-R1). Examination of soluble TNF-R1 production revealed that diseased thyrocytes produced sevenfold more soluble TNF-R1 than normal thyrocytes. Furthermore, basal protein kinase C (pKC) activity in
diseased thyrocytes was 67% higher than that found in normal murine thyrocytes. The elevated basal pKC activity in diseased thyrocytes was related to their enhanced production of soluble TNF-R1 because
inhibition of pKC activity with calphostin C caused soluble TNF-R1 production to decrease significantly. Additionally, soluble TNF-R1 production by murine thyrocytes was not a result of cell-surface receptor
shedding but through secretion of a truncated version of TNF-R1. This was evident when cell-surface TNF-R1 levels were unchanged after treatment of diseased thyrocytes with calphostin C. Also, the 28-kd
form of TNF-R1, which corresponds to the soluble receptor, was present in the intracellular membranes of the diseased thyrocytes.</description><subject>Animals</subject><subject>Cells, Cultured</subject><subject>Disease Models, Animal</subject><subject>Laboratory Research Reports</subject><subject>Mice</subject><subject>Mice, Inbred MRL lpr</subject><subject>Mice, Knockout</subject><subject>Protein Kinase C - metabolism</subject><subject>Receptors, Tumor Necrosis Factor, Type I - biosynthesis</subject><subject>Receptors, Tumor Necrosis Factor, Type I - physiology</subject><subject>Reference Values</subject><subject>Space life sciences</subject><subject>Thyroid Gland - pathology</subject><subject>Thyroid Gland - physiology</subject><subject>Thyroiditis, Autoimmune - enzymology</subject><subject>Thyroiditis, Autoimmune - physiopathology</subject><issn>1050-7256</issn><issn>1557-9077</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkUtLxDAUhYMovv-AC8nKXTWPpmmWw_hEURnHdUnTW4y0jSapMH_FX2vmAS7cuLqXk--cSzgInVByTkmpLigRRDJBcs444USRYgvtUyFkpoiU22lPQJaIYg8dhPBOCC1KyXfRHhU0Z1yU--h7_rbwziwiBHwXXKcjNLj1rseTMTrb9-MA2aUNoEN6WMG2CfgFjIcI-MV1Y90Bno-98_gxqS7YgK-1ic5nM5ocOqZgPIN1dHRJAuvxVQdfK-XZuwh2wPd2SDfwFE9MtF82Lo7QTqu7AMebeYher6_m09vs4enmbjp5yAxTKmZcC5lLwiWhxDSypJSzttVFIbkxutGKCl2XdSEEg5LnihqpIG-pKoHVAhp-iM7WuR_efY4QYtXbYKDr9ABuDJWkihWC5wlka3D5y-ChrT687bVfVJRUy0aqv40k0-kmfax7aH4tmwoSUK6BpayHobNQg4__yf4BnQuYrg</recordid><startdate>20040401</startdate><enddate>20040401</enddate><creator>LaBue, M.</creator><creator>Colburn, K.K.</creator><creator>Green, L.M.</creator><general>Mary Ann Liebert, Inc</general><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>7X8</scope></search><sort><creationdate>20040401</creationdate><title>Thyrocytes Isolated from Autoimmune-Diseased Thyroids Secrete Soluble Tumor Necrosis Factor-R1 That Is Related to Their Elevated Protein Kinase C Activity</title><author>LaBue, M. ; Colburn, K.K. ; Green, L.M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c299t-3a5747037010cd781132ffa6673ccada915ab8b6552e83491c79e4f198e2b5ed3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Animals</topic><topic>Cells, Cultured</topic><topic>Disease Models, Animal</topic><topic>Laboratory Research Reports</topic><topic>Mice</topic><topic>Mice, Inbred MRL lpr</topic><topic>Mice, Knockout</topic><topic>Protein Kinase C - metabolism</topic><topic>Receptors, Tumor Necrosis Factor, Type I - biosynthesis</topic><topic>Receptors, Tumor Necrosis Factor, Type I - physiology</topic><topic>Reference Values</topic><topic>Space life sciences</topic><topic>Thyroid Gland - pathology</topic><topic>Thyroid Gland - physiology</topic><topic>Thyroiditis, Autoimmune - enzymology</topic><topic>Thyroiditis, Autoimmune - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>LaBue, M.</creatorcontrib><creatorcontrib>Colburn, K.K.</creatorcontrib><creatorcontrib>Green, L.M.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Thyroid (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>LaBue, M.</au><au>Colburn, K.K.</au><au>Green, L.M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Thyrocytes Isolated from Autoimmune-Diseased Thyroids Secrete Soluble Tumor Necrosis Factor-R1 That Is Related to Their Elevated Protein Kinase C Activity</atitle><jtitle>Thyroid (New York, N.Y.)</jtitle><addtitle>Thyroid</addtitle><date>2004-04-01</date><risdate>2004</risdate><volume>14</volume><issue>4</issue><spage>249</spage><epage>262</epage><pages>249-262</pages><issn>1050-7256</issn><eissn>1557-9077</eissn><abstract>Soluble tumor necrosis factor (TNF)-α receptors have the potential to modulate TNF-α activity during autoimmune thyroiditis. In this study we examined cell-surface TNF-α receptors and
soluble TNF-α receptor production by thyrocytes from normal and MRL-lpr
-/-
(diseased) mice, which spontaneously develop autoimmune thyroiditis. We found that murine thyrocytes possess the 55-kd receptor
(TNF-R1). Examination of soluble TNF-R1 production revealed that diseased thyrocytes produced sevenfold more soluble TNF-R1 than normal thyrocytes. Furthermore, basal protein kinase C (pKC) activity in
diseased thyrocytes was 67% higher than that found in normal murine thyrocytes. The elevated basal pKC activity in diseased thyrocytes was related to their enhanced production of soluble TNF-R1 because
inhibition of pKC activity with calphostin C caused soluble TNF-R1 production to decrease significantly. Additionally, soluble TNF-R1 production by murine thyrocytes was not a result of cell-surface receptor
shedding but through secretion of a truncated version of TNF-R1. This was evident when cell-surface TNF-R1 levels were unchanged after treatment of diseased thyrocytes with calphostin C. Also, the 28-kd
form of TNF-R1, which corresponds to the soluble receptor, was present in the intracellular membranes of the diseased thyrocytes.</abstract><cop>United States</cop><pub>Mary Ann Liebert, Inc</pub><pmid>15142358</pmid><doi>10.1089/105072504323030906</doi><tpages>14</tpages></addata></record> |
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| ispartof | Thyroid (New York, N.Y.), 2004-04, Vol.14 (4), p.249-262 |
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| language | eng |
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| source | Mary Ann Liebert Online Subscription; MEDLINE |
| subjects | Animals Cells, Cultured Disease Models, Animal Laboratory Research Reports Mice Mice, Inbred MRL lpr Mice, Knockout Protein Kinase C - metabolism Receptors, Tumor Necrosis Factor, Type I - biosynthesis Receptors, Tumor Necrosis Factor, Type I - physiology Reference Values Space life sciences Thyroid Gland - pathology Thyroid Gland - physiology Thyroiditis, Autoimmune - enzymology Thyroiditis, Autoimmune - physiopathology |
| title | Thyrocytes Isolated from Autoimmune-Diseased Thyroids Secrete Soluble Tumor Necrosis Factor-R1 That Is Related to Their Elevated Protein Kinase C Activity |
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