Identification of a LIF-Responsive, Replication-Competent Subpopulation of Human β Cells

Cell Metab. 2020 Feb 4;31(2):327-338.e6. doi: 10.1016/j.cmet.2019.12.009. Epub 2020 Jan 9.

Abstract

The beta (β)-cell mass formed during embryogenesis is amplified by cell replication during fetal and early postnatal development. Thereafter, β cells become functionally mature, and their mass is maintained by a low rate of replication. For those few β cells that replicate in adult life, it is not known how replication is initiated nor whether this occurs in a specialized subset of β cells. We capitalized on a YAP overexpression system to induce replication of stem-cell-derived β cells and, by single-cell RNA sequencing, identified an upregulation of the leukemia inhibitory factor (LIF) pathway. Activation of the LIF pathway induces replication of human β cells in vitro and in vivo. The expression of the LIF receptor is restricted to a subset of transcriptionally distinct human β cells with increased proliferative capacity. This study delineates novel genetic networks that control the replication of LIF-responsive, replication-competent human β cells.

Keywords: CEBPD; LIF; STAT3; beta cells; beta-cell regeneration; beta-cell replication; diabetes; single cell.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Adult
  • Aged
  • Animals
  • B-Lymphocytes / cytology*
  • CCAAT-Enhancer-Binding Protein-delta / metabolism
  • Cell Proliferation*
  • Cells, Cultured
  • Female
  • Humans
  • Leukemia Inhibitory Factor / physiology*
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Inbred NOD
  • Mice, SCID
  • Middle Aged
  • Pluripotent Stem Cells
  • STAT3 Transcription Factor / metabolism
  • Single-Cell Analysis

Substances

  • CEBPD protein, human
  • LIF protein, human
  • Leukemia Inhibitory Factor
  • STAT3 Transcription Factor
  • STAT3 protein, human
  • CCAAT-Enhancer-Binding Protein-delta