Podoplanin is dispensable for mineralized tissue formation and maintenance in the Swiss outbred mouse background.
Alveolar Epithelial Cells
/ metabolism
Animals
Calcification, Physiologic
/ genetics
Cancellous Bone
/ growth & development
Cell Differentiation
/ genetics
Gene Expression Regulation, Developmental
/ genetics
Kidney
/ growth & development
Lung
/ growth & development
Lymph Nodes
/ growth & development
Lymphangiogenesis
/ genetics
Membrane Glycoproteins
/ genetics
Mice
Osteocytes
/ metabolism
Tibia
/ growth & development
Podoplanin
craniofacial development
exercise
osteocyte
skeletogenesis
tooth bud
Journal
Genesis (New York, N.Y. : 2000)
ISSN: 1526-968X
Titre abrégé: Genesis
Pays: United States
ID NLM: 100931242
Informations de publication
Date de publication:
10 2021
10 2021
Historique:
revised:
25
08
2021
received:
02
08
2021
accepted:
26
08
2021
pubmed:
7
9
2021
medline:
1
3
2022
entrez:
6
9
2021
Statut:
ppublish
Résumé
Podoplanin, PDPN, is a mucin-type transmembrane glycoprotein widely expressed in many tissues, including lung, kidney, lymph nodes, and mineralized tissues. Its function is critical for lymphatic formation, differentiation of type I alveolar epithelial lung cells, and for bone response to biomechanical loading. It has previously been shown that Pdpn null mice die at birth due to respiratory failure emphasizing the importance of Pdpn in alveolar lung development. During the course of generation of Pdpn mutant mice, we found that most Pdpn null mice in the 129S6 and C57BL6/J mixed genetic background die at the perinatal stage, similar to previously published studies with Pdpn null mice, while all Pdpn null mice bred with Swiss outbred mice survived. Surviving mutant mice in the 129S6 and C57BL6/J mixed genetic background showed alterations in the osteocyte lacunocanalicular network, especially reduced osteocyte canaliculi in the tibial cortex with increased tibial trabecular bone. However, adult Pdpn null mice in the Swiss outbred background showed no overt differences in their osteocyte lacunocnalicular network, bone density, and no overt differences when challenged with exercise. Together, these data suggest that genetic variations present in the Swiss outbred mice compensate for the loss of function of PDPN in lung, kidney, and bone.
Identifiants
pubmed: 34487426
doi: 10.1002/dvg.23450
pmc: PMC8526399
mid: NIHMS1736789
doi:
Substances chimiques
Gp38 protein, mouse
0
Membrane Glycoproteins
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e23450Subventions
Organisme : NIDCR NIH HHS
ID : R01 DE024797
Pays : United States
Organisme : NIA NIH HHS
ID : P01 AG039355
Pays : United States
Organisme : NIDCR NIH HHS
ID : R01 DE020843
Pays : United States
Organisme : NIAMS NIH HHS
ID : P30 AR069620
Pays : United States
Organisme : NIDCR NIH HHS
ID : R03 DE027456
Pays : United States
Informations de copyright
© 2021 Wiley Periodicals LLC.
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