Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2002-3-21
pubmed:abstractText
The secretion and localization of clusterin in the testis has led to the hypothesis that clusterin plays a role in spermatogenesis. Furthermore, the association of clusterin with apoptosis, cellular injury, disease, and regression of nongonadal tissues has led to the hypothesis that clusterin acts to protect cells from apoptosis or may be involved in tissue remodeling. To investigate the role of clusterin in the testis, we analyzed clusterin knock-out (cluKO) mice to determine the impact of the absence of clusterin on spermatogenesis. Furthermore, we investigated the cellular response to injury caused by methoxyacetic acid (MAA) toxicity and mild heat exposure in the cluKO mice to determine the extent to which clusterin protects against apoptosis or participates in tissue remodeling. We found that cluKO mice were fertile and had essentially normal spermatogenesis with the exception of some incomplete spermiation after stage VIII. No differences in testicular morphology or the incidence of apoptosis in the testis were seen between the cluKO and clusterin wild-type (cluWT) mice after MAA treatment. In contrast, apoptosis was delayed in the cluWT mice compared with the cluKO mice after heat exposure, suggesting that clusterin does have a slight protective effect against apoptosis under some conditions. Also, a dramatic loss of germ cells after heat stress occurred earlier in the cluWT testes than in the cluKO testes. Clusterin is clearly acting in a dual role in that cells can be protected from damage and dead cells can be more easily removed after some types of cellular damage but not after others.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0006-3363
pubmed:author
pubmed:issnType
Print
pubmed:volume
66
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1042-53
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:11906924-Acetic Acids, pubmed-meshheading:11906924-Animals, pubmed-meshheading:11906924-Apoptosis, pubmed-meshheading:11906924-Clusterin, pubmed-meshheading:11906924-Cytoplasm, pubmed-meshheading:11906924-DNA Fragmentation, pubmed-meshheading:11906924-Female, pubmed-meshheading:11906924-Glycoproteins, pubmed-meshheading:11906924-Hot Temperature, pubmed-meshheading:11906924-Immunohistochemistry, pubmed-meshheading:11906924-In Situ Nick-End Labeling, pubmed-meshheading:11906924-Male, pubmed-meshheading:11906924-Mice, pubmed-meshheading:11906924-Mice, Knockout, pubmed-meshheading:11906924-Molecular Chaperones, pubmed-meshheading:11906924-Organ Size, pubmed-meshheading:11906924-Sertoli Cells, pubmed-meshheading:11906924-Sperm Count, pubmed-meshheading:11906924-Spermatogenesis, pubmed-meshheading:11906924-Spermatozoa, pubmed-meshheading:11906924-Testis
pubmed:year
2002
pubmed:articleTitle
Heat shock-initiated apoptosis is accelerated and removal of damaged cells is delayed in the testis of clusterin/ApoJ knock-out mice.
pubmed:affiliation
School of Molecular Biosciences, Center for Reproductive Biology, Washington State University, Pullman, WA 99164-4660, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.