The Adult Murine Intestine is Dependent on Constitutive Laminin-γ1 Synthesis.
British FieldsAnn DeLaForestMark ZoggJennifer MayCatherine HagenKristin KomnickJon WieserAlexander LundbergHartmut WeilerMichele A BattleKaren-Sue Barker CarlsonPublished in: Scientific reports (2019)
Laminin-γ1 is required for early embryonic development; however, the need for laminin-γ1 synthesis in adulthood is unknown. A global and inducible mouse model of laminin-γ1 deficiency was generated to address this question. Genetic ablation of the Lamc1 gene in adult mice was rapidly lethal. Despite global Lamc1 gene deletion in tamoxifen-induced mutant mice, there was minimal change in total cardiac, pulmonary, hepatic or renal laminin protein. In contrast, laminin-γ1 was significantly depleted in the small intestines, which showed crypt hyperplasia and dissociation of villous epithelium from adjacent mesenchyme. We conclude that the physiologic requirement for laminin-γ1 synthesis in adult mice is dependent on a tissue-specific basal rate of laminin-γ1 turnover that results in rapid depletion of laminin-γ1 in the intestine.
Keyphrases
- mouse model
- genome wide
- copy number
- heart failure
- depressive symptoms
- type diabetes
- magnetic resonance imaging
- pulmonary hypertension
- magnetic resonance
- dna methylation
- gene expression
- oxidative stress
- skeletal muscle
- adipose tissue
- transcription factor
- insulin resistance
- endothelial cells
- body composition
- high glucose
- breast cancer cells
- binding protein
- diabetic rats
- early life