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Insulin cell mass is altered in Csf1 op /Csf1 op macrophage‐deficient mice
Author(s) -
BanaeiBouchareb Linda,
GouonEvans Valerie,
SamaraBoustani Dinane,
Castellotti Marie Claire,
Czernichow Paul,
Pollard Jeffrey W.,
Polak Michel
Publication year - 2004
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.1103591
Subject(s) - biology , endocrinology , pancreas , medicine , macrophage , neogenesis , insulin , islet , glucose homeostasis , pancreatic islets , fetus , pregnancy , insulin resistance , biochemistry , in vitro , genetics
Macrophages play an important role in organ development, tissue homeostasis, and remodeling. Thus, we monitored the presence of F4/80‐positive macrophages in the pancreas of wild‐type mice, and some developmental features of this complex tissue were compared throughout life in wild‐type and macrophage‐deficient Csf1 op /Csf1 op (op/op) mice. The combined use of immunohistochemistry, morphometry, and cell quantification allows us to evaluate insulin and glucagon cell mass, total and insulin cell proliferation, and apoptosis in fetuses (E18.5), weanings (postnatal day 21), nonpregnant adults, and adults in late pregnancy (18.5 days). F4/80‐positive macrophages were found in pancreases recovered from Csf1 op /Csf1 + (op/+) mice but were extremely scarce or absent in pancreas recovered from op/op ones at all studied time‐points. The macrophage‐deficient op/op phenotype was clearly associated with a major insulin mass deficit in fetuses and adults, abnormal postnatal islet morphogenesis, and impaired pancreatic cell proliferation at weaning and late pregnancy. We also obtained indirect evidence of increased neogenesis in this model at time‐points when pancreatic remodeling does occur. The demonstration of the colony‐stimulating factor 1‐dependent macrophage involvement in life‐time pancreas development/remodeling allows us to pinpoint the tissue‐modeling and remodeling functions of this leukocyte lineage.