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Pancreatic Exocrine Tissue Architecture and Integrity are Maintained by E-cadherin During Postnatal Development
Jeffrey D Serrill1, Maike Sander2, Hung Ping Shih3
1Department of Translational Research and Cellular Therapeutics, Diabetes and Metabolic Research Institute, Beckman Research Institute, City of Hope, Duarte, CA, 91010, USA.
Scientific Reports
|September 9, 2018
Summary
E-cadherin is crucial for maintaining pancreatic structure and function after birth. Its absence leads to acinar-to-ductal metaplasia and signaling dysregulation, impacting organ development and potentially causing disease.
Area of Science:
- Cell Biology
- Developmental Biology
- Organogenesis
Background:
- Cadherin-mediated cell-cell adhesion is vital for organ development.
- Changes in cadherin expression are linked to morphogenetic and pathogenic events.
- E-cadherin (Cdh1) is a key component of adherens junctions, providing mechanical cell attachments.
Purpose of the Study:
- To investigate the role of E-cadherin in the developing pancreas.
- To understand the consequences of E-cadherin deficiency in pancreatic architecture and signaling.
Main Methods:
- Generation and analysis of pancreas-specific Cdh1-knockout (Cdh1 ΔPan/ΔPan ) mice.
- Assessment of body weight, blood glucose, pancreatic architecture, and signaling pathways (Wnt, YAP).
Main Results:
- Cdh1 ΔPan/ΔPan mice showed normal birth size but failed to gain weight and became hypoglycemic.
- E-cadherin was not essential for initial polarity or exocrine cell identity.
- Progressive deterioration of exocrine architecture and ductal metaplasia were observed postnatally.
- Dysregulation of Wnt and YAP signaling pathways occurred in E-cadherin-deficient pancreata.
Conclusions:
- E-cadherin is essential for maintaining pancreatic exocrine architecture and regulating homeostatic signaling postnatally.
- E-cadherin deficiency can lead to acinar-to-ductal metaplasia (ADM).
- This study highlights E-cadherin's role in pancreatic health and disease, including pancreatitis and cancer.
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