4.7 Article

Djhsp60 Is Required for Planarian Regeneration and Homeostasis

期刊

BIOMOLECULES
卷 12, 期 6, 页码 -

出版社

MDPI
DOI: 10.3390/biom12060808

关键词

planarian; regeneration; HSP60; mitochondria; cathepsin L

资金

  1. National Natural Science Foundation of China [31572267, 31471965]
  2. Doctoral Scientific Research Start-up Foundation of Luohe Medical College [2021-DF-01]

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This study investigates the role of HSP60 in tissue regeneration and homeostasis using freshwater planarians as a model system. HSP60 is found in all types of cells, but is particularly abundant in stem cells and head neural cells. Knockdown of HSP60 leads to head regression and loss of regenerating abilities, as well as disruption of mitochondrial structure and inhibition of intestinal tissue function.
HSP60, a well-known mitochondrial chaperone, is essential for mitochondrial homeostasis. HSP60 deficiency causes dysfunction of the mitochondria and is lethal to animal survival. Here, we used freshwater planarian as a model system to investigate and uncover the roles of HSP60 in tissue regeneration and homeostasis. HSP60 protein is present in all types of cells in planarians, but it is relatively rich in stem cells and head neural cells. Knockdown of HSP60 by RNAi causes head regression and the loss of regenerating abilities, which is related to decrease in mitotic cells and inhibition of stem cell-related genes. RNAi-HSP60 disrupts the structure of the mitochondria and inhibits the mitochondrial-related genes, which mainly occur in intestinal tissues. RNAi-HSP60 also damages the integrity of intestinal tissues and downregulates intestine-expressed genes. More interestingly, RNAi-HSP60 upregulates the expression of the cathepsin L-like gene, which may be the reason for head regression and necrotic-like cell death. Taking these points together, we propose a model illustrating the relationship between neoblasts and intestinal cells, and also highlight the essential role of the intestinal system in planarian regeneration and tissue homeostasis.

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