Indispensable role of Galectin-3 in promoting quiescence of hematopoietic stem cells

Weizhen Jia, Lingyu Kong, Hiroyasu Kidoya, Hisamichi Naito, Fumitaka Muramatsu, Yumiko Hayashi, Han-Yun Hsieh, Daishi Yamakawa, Daniel K. Hsu, Fu-Tong Liu and Nobuyuki Takakura ()
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Weizhen Jia: Osaka University, Suita
Lingyu Kong: Harbin Medical University Cancer Hospital
Hiroyasu Kidoya: Osaka University, Suita
Hisamichi Naito: Osaka University, Suita
Fumitaka Muramatsu: Osaka University, Suita
Yumiko Hayashi: Osaka University, Suita
Han-Yun Hsieh: Osaka University, Suita
Daishi Yamakawa: Mie University Graduate School of Medicine
Daniel K. Hsu: University of California-Davis
Fu-Tong Liu: University of California-Davis
Nobuyuki Takakura: Osaka University, Suita

Nature Communications, 2021, vol. 12, issue 1, 1-17

Abstract: Abstract Hematopoietic stem cells (HSCs) in adult bone marrow (BM) are usually maintained in a state of quiescence. The cellular mechanism coordinating the balance between HSC quiescence and differentiation is not fully understood. Here, we report that galactose-binding lectin-3 (galectin-3; Gal-3) is upregulated by Tie2 or Mpl activation to maintain quiescence. Conditional overexpression of Gal-3 in mouse HSCs under the transcriptional control of Tie2 or Vav1 promoters (Gal-3 Tg) causes cell cycle retardation via induction of p21. Conversely, the cell cycle of long-term repopulating HSCs (LT-HSCs) in Gal-3-deficient (Gal-3-/-) mice is accelerated, resulting in their exhaustion. Mechanistically, Gal-3 regulates p21 transcription by forming a complex with Sp1, thus blocking cell cycle entry. These results demonstrate that Gal-3 is a negative regulator of cell-cycling in HSCs and plays a crucial role in adult hematopoiesis to prevent HSC exhaustion.

Date: 2021
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DOI: 10.1038/s41467-021-22346-2

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