Impaired wound healing in mice lacking the basement membrane protein nidogen 1.
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Impaired wound healing in mice lacking the basement membrane protein nidogen 1. / Baranowsky, Anke; Mokkapati, Sharada; Bechtel, Manuela; Krügel, Jenny; Miosge, Nicolai; Wickenhauser, Claudia; Smyth, Neil; Nischt, Roswitha.
In: MATRIX BIOL, Vol. 29, No. 1, 1, 2010, p. 15-21.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - Impaired wound healing in mice lacking the basement membrane protein nidogen 1.
AU - Baranowsky, Anke
AU - Mokkapati, Sharada
AU - Bechtel, Manuela
AU - Krügel, Jenny
AU - Miosge, Nicolai
AU - Wickenhauser, Claudia
AU - Smyth, Neil
AU - Nischt, Roswitha
PY - 2010
Y1 - 2010
N2 - Nidogens 1 and 2 are ubiquitous basement membrane (BM) components, whose interactions in particular with laminin, collagen IV and perlecan have been considered important for BM formation. Genetic deletion of either NID gene does not reveal BM alterations suggesting compensatory roles for nidogens 1 and 2. However, neurological deficits in nidogen 1 null mice, not seen in the absence of nidogen 2, also suggest isoform specific functions. To test this further, skin wound healing which requires BM reformation was studied in adult nidogen 1 deficient mice. Although re-epithelialization was not altered, the newly formed epidermis showed marked hyperproliferation and a delay in differentiation at day 10 post injury. Distinct to control wounds, there was also considerable alpha-smooth muscle actin staining in the dermis of nidogen 1 deficient wounds at this time point. Further, laminin deposition and distribution of the beta1 and beta4 integrin chains were also significantly altered whereas the deposition of other BM components, including nidogen 2, was unchanged. Surprisingly, these differences between control and mutant wounds at day 10 post wounding did not affect the ultrastructural appearance of the dermo-epidermal BM suggesting a non-structural role for nidogen 1 in wound repair.
AB - Nidogens 1 and 2 are ubiquitous basement membrane (BM) components, whose interactions in particular with laminin, collagen IV and perlecan have been considered important for BM formation. Genetic deletion of either NID gene does not reveal BM alterations suggesting compensatory roles for nidogens 1 and 2. However, neurological deficits in nidogen 1 null mice, not seen in the absence of nidogen 2, also suggest isoform specific functions. To test this further, skin wound healing which requires BM reformation was studied in adult nidogen 1 deficient mice. Although re-epithelialization was not altered, the newly formed epidermis showed marked hyperproliferation and a delay in differentiation at day 10 post injury. Distinct to control wounds, there was also considerable alpha-smooth muscle actin staining in the dermis of nidogen 1 deficient wounds at this time point. Further, laminin deposition and distribution of the beta1 and beta4 integrin chains were also significantly altered whereas the deposition of other BM components, including nidogen 2, was unchanged. Surprisingly, these differences between control and mutant wounds at day 10 post wounding did not affect the ultrastructural appearance of the dermo-epidermal BM suggesting a non-structural role for nidogen 1 in wound repair.
M3 - SCORING: Zeitschriftenaufsatz
VL - 29
SP - 15
EP - 21
JO - MATRIX BIOL
JF - MATRIX BIOL
SN - 0945-053X
IS - 1
M1 - 1
ER -
