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Article: Expression of transforming growth factor alpha and epidermal growth factor receptor in adult polycystic kidney disease

TitleExpression of transforming growth factor alpha and epidermal growth factor receptor in adult polycystic kidney disease
Authors
KeywordsAdult polycystic kidney disease
Epidermal growth factor receptor
Transforming growth factor alpha
Issue Date1998
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.elsevier.com/locate/juro
Citation
Journal Of Urology, 1998, v. 159 n. 1, p. 291-296 How to Cite?
AbstractAdult polycystic kidney disease (APKD) is a common genetic disease with a frequency of 1:1000. Evidence suggests that transforming growth factor alpha (TGFα) signaling may contribute to the hyperproliferation of the cystic epithelia in APKD. TGFα and epidermal growth factor (EGF) are well known mitogens expressed in the kidney and both exert their biological activities through binding to the same EGF receptor. A transgenic mouse that over-expressed TGFα developed renal cysts; raised levels of TGFα and EGF receptor mRNA were found in kidneys from two autosomal dominant APKD patients. To study the role of TGFα in cyst formation, we analyzed nine anatomically diagnosed adult polycystic kidneys and four normal kidneys using immunohistochemistry. We also traced the possible origins of the cysts by staining with the proximal convoluted tubule (PCT) marker, gp330, and the distal convoluted tubule (DCT) and collecting tubule (CT) marker, peanut agglutinin (PNA). In normal kidneys, TGFα protein was concentrated in the DCT and CT and EGF receptor protein in all three tubule types. In the early cysts of APKD, the cystic epithelia showed strong positive staining with TGFα, EGF receptor and gp330 but negative with PNA. Strong TGFα and EGF receptor staining was also found in the mixture of advanced cysts in the end- stage cystic kidneys although the cysts are likely to be derived from different segments of the renal tubules. This increased TGFα and EGF receptor expression in all cases and all types of cysts suggests that autocrine/paracrine stimulation by TGFα may be a common mechanism in cyst development in APKD.
Persistent Identifierhttp://hdl.handle.net/10722/80148
ISSN
2023 Impact Factor: 5.9
2023 SCImago Journal Rankings: 1.938
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLee, DCWen_HK
dc.contributor.authorChan, KWen_HK
dc.contributor.authorChan, SYen_HK
dc.date.accessioned2010-09-06T08:02:58Z-
dc.date.available2010-09-06T08:02:58Z-
dc.date.issued1998en_HK
dc.identifier.citationJournal Of Urology, 1998, v. 159 n. 1, p. 291-296en_HK
dc.identifier.issn0022-5347en_HK
dc.identifier.urihttp://hdl.handle.net/10722/80148-
dc.description.abstractAdult polycystic kidney disease (APKD) is a common genetic disease with a frequency of 1:1000. Evidence suggests that transforming growth factor alpha (TGFα) signaling may contribute to the hyperproliferation of the cystic epithelia in APKD. TGFα and epidermal growth factor (EGF) are well known mitogens expressed in the kidney and both exert their biological activities through binding to the same EGF receptor. A transgenic mouse that over-expressed TGFα developed renal cysts; raised levels of TGFα and EGF receptor mRNA were found in kidneys from two autosomal dominant APKD patients. To study the role of TGFα in cyst formation, we analyzed nine anatomically diagnosed adult polycystic kidneys and four normal kidneys using immunohistochemistry. We also traced the possible origins of the cysts by staining with the proximal convoluted tubule (PCT) marker, gp330, and the distal convoluted tubule (DCT) and collecting tubule (CT) marker, peanut agglutinin (PNA). In normal kidneys, TGFα protein was concentrated in the DCT and CT and EGF receptor protein in all three tubule types. In the early cysts of APKD, the cystic epithelia showed strong positive staining with TGFα, EGF receptor and gp330 but negative with PNA. Strong TGFα and EGF receptor staining was also found in the mixture of advanced cysts in the end- stage cystic kidneys although the cysts are likely to be derived from different segments of the renal tubules. This increased TGFα and EGF receptor expression in all cases and all types of cysts suggests that autocrine/paracrine stimulation by TGFα may be a common mechanism in cyst development in APKD.en_HK
dc.languageengen_HK
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.elsevier.com/locate/juroen_HK
dc.relation.ispartofJournal of Urologyen_HK
dc.rightsThe Journal of Urology. Copyright © Lippincott Williams & Wilkins.en_HK
dc.subjectAdult polycystic kidney diseaseen_HK
dc.subjectEpidermal growth factor receptoren_HK
dc.subjectTransforming growth factor alphaen_HK
dc.subject.meshAdulten_HK
dc.subject.meshAgeden_HK
dc.subject.meshFemaleen_HK
dc.subject.meshHumansen_HK
dc.subject.meshKidney - metabolismen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiddle Ageden_HK
dc.subject.meshPolycystic Kidney Diseases - metabolismen_HK
dc.subject.meshReceptor, Epidermal Growth Factor - metabolismen_HK
dc.subject.meshTransforming Growth Factor alpha - metabolismen_HK
dc.titleExpression of transforming growth factor alpha and epidermal growth factor receptor in adult polycystic kidney diseaseen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0022-5347&volume=159&spage=291&epage=296&date=1998&atitle=Expression+of+Transforming+Growth+Factor+Alpha+and+Epidermal+Growth+Factor+Receptor+in+Adult+Polycystic+Kidney+Diseaseen_HK
dc.identifier.emailChan, KW:hrmtckw@hku.hken_HK
dc.identifier.emailChan, SY:sychan@hkucc.hku.hken_HK
dc.identifier.authorityChan, KW=rp00330en_HK
dc.identifier.authorityChan, SY=rp00356en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/S0022-5347(01)64084-9-
dc.identifier.pmid9400497-
dc.identifier.scopuseid_2-s2.0-0031986343en_HK
dc.identifier.hkuros30062en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0031986343&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume159en_HK
dc.identifier.issue1en_HK
dc.identifier.spage291en_HK
dc.identifier.epage296en_HK
dc.identifier.isiWOS:A1998YK23200091-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridLee, DCW=7406663288en_HK
dc.identifier.scopusauthoridChan, KW=16444133100en_HK
dc.identifier.scopusauthoridChan, SY=7404255082en_HK
dc.identifier.issnl0022-5347-

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