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LSD1 inhibition yields functional insulin-producing cells from human embryonic stem cells
Fei He1,2, Ning Li1,2, Hai-Bo Huang1,2
1Translational Medicine Collaborative Innovation Center, The Second Clinical Medical College (Shenzhen People's Hospital), Jinan University, 1017 Dongmen North Road, Shenzhen, 518020, China.
Stem Cell Research & Therapy
|April 30, 2020
Summary
Inhibiting lysine-specific demethylase 1 (LSD1) promotes human embryonic stem cell differentiation into insulin-producing cells. This finding offers a new therapeutic strategy for diabetes by enhancing pancreatic beta cell generation.
Area of Science:
- Stem cell biology
- Endocrinology
- Molecular biology
Background:
- Human embryonic stem cells (hESCs) offer a promising source for insulin-producing cells (IPCs) for diabetes therapy.
- Understanding the mechanisms regulating hESC differentiation into IPCs is crucial.
- Lysine-specific demethylase 1 (LSD1) is known to regulate self-renewal and differentiation in stem cells.
Purpose of the Study:
- To investigate the role of LSD1 in the directed differentiation of hESCs into IPCs.
- To explore LSD1 inhibition as a potential therapeutic approach for diabetes.
Main Methods:
- Directed differentiation of H9 hESC line into IPCs using a four-step protocol.
- Lentivirus-mediated knockdown of LSD1 expression.
- Immunofluorescence, flow cytometry, Western blot, and ELISA were used to assess differentiation efficiency, signaling pathways, and insulin secretion.
Main Results:
- LSD1 inhibition or silencing enhanced pancreatic progenitor specification and commitment to functional IPCs.
- LSD1 inhibition activated ERK signaling and upregulated pancreatic progenitor genes, promoting maturation and proliferation.
- IPCs treated with an LSD1 inhibitor showed improved glucose-stimulated insulin secretion.
Conclusions:
- LSD1 inhibition is a novel strategy to promote IPC differentiation from hESCs.
- This approach holds potential for generating functional pancreatic beta cells for diabetes treatment.
