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cr uuu---uuuuu |
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231224s2013 xx |||||o 00| ||eng c |
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|a 10.1016/j.clim.2013.03.001
|2 doi
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|a pubmed24n0755.xml
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|a (DE-627)NLM22653426X
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|a (NLM)23571102
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|a (PII)S1521-6616(13)00060-0
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|a DE-627
|b ger
|c DE-627
|e rakwb
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|a eng
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| 100 |
1 |
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|a Ota, Yuko
|e verfasserin
|4 aut
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| 245 |
1 |
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|a Ghrelin attenuates collagen production in lesional fibroblasts from patients with systemic sclerosis
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|c 2013
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| 336 |
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|a Text
|b txt
|2 rdacontent
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|a ƒaComputermedien
|b c
|2 rdamedia
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| 338 |
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|a ƒa Online-Ressource
|b cr
|2 rdacarrier
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| 500 |
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|a Date Completed 20.06.2013
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|a Date Revised 02.12.2018
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|a published: Print-Electronic
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|a Citation Status MEDLINE
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|a Copyright © 2013 Elsevier Inc. All rights reserved.
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|a Systemic sclerosis (SSc) is a connective tissue disease characterized by thickening of the skin and tissue fibrosis of the internal organs. Ghrelin is primarily described as a gut hormone, and many studies currently indicate that ghrelin has protective effects in different organs, including the heart, pancreas, lung and liver, resulting from its anti-fibrotic properties. We found decreased levels of ghrelin in the plasma from patients with SSc compared with those from healthy controls. In skin fibroblast cultures, recombinant ghrelin diminished the production of collagen type I. In addition, the mRNA levels of COL1A2 and TGFB genes were significantly decreased by the stimulation of ghrelin. We showed that ghrelin may exert anti-fibrotic effects in the skin fibroblasts from patients with SSc. Because the plasma levels of ghrelin are low in SSc, the administration of ghrelin could be a new strategy for the treatment of SSc
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|a Journal Article
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|a Research Support, Non-U.S. Gov't
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|a Autoantibodies
|2 NLM
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| 650 |
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|a Collagen Type I
|2 NLM
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| 650 |
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|a Ghrelin
|2 NLM
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| 650 |
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|a RNA, Messenger
|2 NLM
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| 650 |
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|a Receptors, Ghrelin
|2 NLM
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| 650 |
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|a TGFB1 protein, human
|2 NLM
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| 650 |
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|a Transforming Growth Factor beta1
|2 NLM
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| 700 |
1 |
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|a Kawaguchi, Yasushi
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Takagi, Kae
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Ichida, Hisae
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Gono, Takahisa
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Hanaoka, Masanori
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Higuchi, Tomoaki
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Yamanaka, Hisashi
|e verfasserin
|4 aut
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| 773 |
0 |
8 |
|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 147(2013), 2 vom: 15. Mai, Seite 71-8
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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|g volume:147
|g year:2013
|g number:2
|g day:15
|g month:05
|g pages:71-8
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|u http://dx.doi.org/10.1016/j.clim.2013.03.001
|3 Volltext
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