Mouse Models of Human Claudin-Associated Disorders: Benefits and Limitations

In higher organisms, epithelia separate compartments in order to guarantee their proper function. Such structures are able to seal but also to allow substances to pass. Within the paracellular pathway, a supramolecular structure, the tight junction transport is largely controlled by the temporospati...

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Vydáno v:International journal of molecular sciences Ročník 20; číslo 21; s. 5504
Hlavní autoři: Seker, Murat, Fernández-Rodríguez, Cármen, Martínez-Cruz, Luis, Müller, Dominik
Médium: Journal Article
Jazyk:angličtina
Vydáno: Switzerland MDPI AG 05.11.2019
MDPI
Témata:
Alopecia
Amino Acid Sequence
Animals
Baldness
Cholangitis
Claudins - chemistry
Claudins - genetics
Colorectal cancer
Disease Models, Animal
Eye Diseases - genetics
Gene expression
Hepatitis
Humans
Inflammatory bowel disease
Kidney Diseases - genetics
Liver
Liver Diseases - genetics
Mice
Morphology
Mutation
Neoplasms - genetics
Pathophysiology
Physiology
Proteins
Review
Rodents
Skin
Skin Diseases - genetics
Stem cells
kidney
disease
mutations
liver
skin
claudin
human
mice
tight junction
ISSN:1422-0067, 1661-6596, 1422-0067
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Abstract In higher organisms, epithelia separate compartments in order to guarantee their proper function. Such structures are able to seal but also to allow substances to pass. Within the paracellular pathway, a supramolecular structure, the tight junction transport is largely controlled by the temporospatial regulation of its major protein family called claudins. Besides the fact that the expression of claudins has been identified in different forms of human diseases like cancer, clearly defined mutations in the corresponding claudin genes have been shown to cause distinct human disorders. Such disorders comprise the skin and its adjacent structures, liver, kidney, the inner ear, and the eye. From the phenotype analysis, it has also become clear that different claudins can cause a complex phenotype when expressed in different organs. To gain deeper insights into the physiology and pathophysiology of claudin-associated disorders, several mouse models have been generated. In order to model human disorders in detail, they have been designed either as full knockouts, knock-downs or knock-ins by a variety of techniques. Here, we review human disorders caused by CLDN mutations and their corresponding mouse models that have been generated thus far and assess their usefulness as a model for the corresponding human disorder.
AbstractList In higher organisms, epithelia separate compartments in order to guarantee their proper function. Such structures are able to seal but also to allow substances to pass. Within the paracellular pathway, a supramolecular structure, the tight junction transport is largely controlled by the temporospatial regulation of its major protein family called claudins. Besides the fact that the expression of claudins has been identified in different forms of human diseases like cancer, clearly defined mutations in the corresponding claudin genes have been shown to cause distinct human disorders. Such disorders comprise the skin and its adjacent structures, liver, kidney, the inner ear, and the eye. From the phenotype analysis, it has also become clear that different claudins can cause a complex phenotype when expressed in different organs. To gain deeper insights into the physiology and pathophysiology of claudin-associated disorders, several mouse models have been generated. In order to model human disorders in detail, they have been designed either as full knockouts, knock-downs or knock-ins by a variety of techniques. Here, we review human disorders caused by CLDN mutations and their corresponding mouse models that have been generated thus far and assess their usefulness as a model for the corresponding human disorder.In higher organisms, epithelia separate compartments in order to guarantee their proper function. Such structures are able to seal but also to allow substances to pass. Within the paracellular pathway, a supramolecular structure, the tight junction transport is largely controlled by the temporospatial regulation of its major protein family called claudins. Besides the fact that the expression of claudins has been identified in different forms of human diseases like cancer, clearly defined mutations in the corresponding claudin genes have been shown to cause distinct human disorders. Such disorders comprise the skin and its adjacent structures, liver, kidney, the inner ear, and the eye. From the phenotype analysis, it has also become clear that different claudins can cause a complex phenotype when expressed in different organs. To gain deeper insights into the physiology and pathophysiology of claudin-associated disorders, several mouse models have been generated. In order to model human disorders in detail, they have been designed either as full knockouts, knock-downs or knock-ins by a variety of techniques. Here, we review human disorders caused by CLDN mutations and their corresponding mouse models that have been generated thus far and assess their usefulness as a model for the corresponding human disorder.
In higher organisms, epithelia separate compartments in order to guarantee their proper function. Such structures are able to seal but also to allow substances to pass. Within the paracellular pathway, a supramolecular structure, the tight junction transport is largely controlled by the temporospatial regulation of its major protein family called claudins. Besides the fact that the expression of claudins has been identified in different forms of human diseases like cancer, clearly defined mutations in the corresponding claudin genes have been shown to cause distinct human disorders. Such disorders comprise the skin and its adjacent structures, liver, kidney, the inner ear, and the eye. From the phenotype analysis, it has also become clear that different claudins can cause a complex phenotype when expressed in different organs. To gain deeper insights into the physiology and pathophysiology of claudin-associated disorders, several mouse models have been generated. In order to model human disorders in detail, they have been designed either as full knockouts, knock-downs or knock-ins by a variety of techniques. Here, we review human disorders caused by CLDN mutations and their corresponding mouse models that have been generated thus far and assess their usefulness as a model for the corresponding human disorder.
Author Martínez-Cruz, Luis
Müller, Dominik
Fernández-Rodríguez, Cármen
Seker, Murat
AuthorAffiliation 1 Department of Pediatric Gastroenterology, Nephrology and Metabolism, Charité—Universitätsmedizin Berlin, Charité, 13353 Berlin, Germany; murat.seker@charite.de
2 ClC BioGUNE, Bizkaia Science and Technology Park, 801A, 48160 Derio, Spain; cfernandez@cicbiogune.es (C.F.-R.); amartinez@cicbiogune.es (L.A.M.-C.)
AuthorAffiliation_xml – name: 1 Department of Pediatric Gastroenterology, Nephrology and Metabolism, Charité—Universitätsmedizin Berlin, Charité, 13353 Berlin, Germany; murat.seker@charite.de
– name: 2 ClC BioGUNE, Bizkaia Science and Technology Park, 801A, 48160 Derio, Spain; cfernandez@cicbiogune.es (C.F.-R.); amartinez@cicbiogune.es (L.A.M.-C.)
Author_xml – sequence: 1
  givenname: Murat
  orcidid: 0000-0003-2306-6005
  surname: Seker
  fullname: Seker, Murat
– sequence: 2
  givenname: Cármen
  surname: Fernández-Rodríguez
  fullname: Fernández-Rodríguez, Cármen
– sequence: 3
  givenname: Luis
  orcidid: 0000-0002-5856-9377
  surname: Martínez-Cruz
  fullname: Martínez-Cruz, Luis
– sequence: 4
  givenname: Dominik
  orcidid: 0000-0002-3478-1576
  surname: Müller
  fullname: Müller, Dominik
BackLink https://www.ncbi.nlm.nih.gov/pubmed/31694170$$D View this record in MEDLINE/PubMed
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Issue 21
Keywords kidney
disease
mutations
liver
skin
claudin
human
mice
tight junction
Language English
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SubjectTerms Alopecia
Amino Acid Sequence
Animals
Baldness
Cholangitis
Claudins - chemistry
Claudins - genetics
Colorectal cancer
Disease Models, Animal
Eye Diseases - genetics
Gene expression
Hepatitis
Humans
Inflammatory bowel disease
Kidney Diseases - genetics
Liver
Liver Diseases - genetics
Mice
Morphology
Mutation
Neoplasms - genetics
Pathophysiology
Physiology
Proteins
Review
Rodents
Skin
Skin Diseases - genetics
Stem cells
Title Mouse Models of Human Claudin-Associated Disorders: Benefits and Limitations
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https://pubmed.ncbi.nlm.nih.gov/PMC6862546
Volume 20
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