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- Title
Localization and potential function of kindlin-1 in periodontal tissues.
- Authors
Petricca, Giorgio; Leppilampi, Mari; Jiang, Guoqiao; Owen, Gethin R.; Wiebe, Colin; Tu, Yizeng; Koivisto, Leeni; Häkkinen, Lari; Wu, Chuanyue; Larjava, Hannu
- Abstract
Kindlin-1 is an intracellular focal adhesion protein that regulates the actin cytoskeleton. Patients suffering from Kindler syndrome have a homologous mutation of the kindlin-1 gene and develop skin blisters, periodontal disease, and intestinal complications because of deficient adhesion of the basal epithelial cells. We investigated kindlin-1 localization in periodontal tissue and its functions in cultured keratinocytes and showed that kindlin-1 co-localizes with migfilin and paxillin in the basal epithelial cells of oral mucosa and in cultured keratinocytes. The kindlin-1-deficient oral mucosal tissue from a patient with Kindler syndrome showed a complete lack of paxillin and reduced migfilin immunostaining in the basal keratinocytes. Co-immunoprecipitation showed that migfilin directly interacted with kindlin-1. RNA interference-induced kindlin-1 deficiency in keratinocytes led to an altered distribution of migfilin-containing focal adhesions, reduced cell spreading, decreased cell proliferation, and decelerated cell migration. Disruption of microtubules in the kindlin-1-deficient cells further reduced cell spreading, suggesting that microtubules can partially compensate for kindlin-1 deficiency. Kindlin-1 supported mature cell–extracellular matrix adhesions of keratinocytes, as downregulation of kindlin-1 expression significantly reduced the cell-adhesion strength. In summary, kindlin-1 interacts with migfilin and plays a crucial role in actin-dependent keratinocyte cell adhesion essential for epidermal and periodontal health.
- Subjects
KERATINOCYTES; EPITHELIAL cells; CELL growth; CELL proliferation; PERIODONTICS
- Publication
European Journal of Oral Sciences, 2009, Vol 117, Issue 5, p518
- ISSN
0909-8836
- Publication type
Article
- DOI
10.1111/j.1600-0722.2009.00651.x