Secretory leukocyte protease inhibitor in the cervical mucus and in the fetal membranes

1995 ◽  
Vol 59 (1) ◽  
pp. 95-101 ◽  
Author(s):  
R. Helmig ◽  
N. Uldbjerg ◽  
K. Ohlsson
Keyword(s):  
Protease Inhibitor ◽  
Secretory Leukocyte Protease Inhibitor ◽  
Cervical Mucus ◽  
Fetal Membranes

Elevated concentration of secretory leukocyte protease inhibitor in the cervical mucus before delivery

2016 ◽  
Vol 214 (6) ◽  
pp. 741.e1-741.e7 ◽  
Author(s):  
Taiki Samejima ◽  
Takeshi Nagamatsu ◽  
Danny J. Schust ◽  
Nao Itaoka ◽  
Takayuki Iriyama ◽  
...  
Keyword(s):  
Protease Inhibitor ◽  
Secretory Leukocyte Protease Inhibitor ◽  
Cervical Mucus ◽  
Elevated Concentration

Evaluation of the levels of secretory leukocyte protease inhibitor in the cervical mucus of women with unexplained infertility

2020 ◽  
Vol 46 (7) ◽  
pp. 1128-1132
Author(s):  
Ilknur Col Madendag ◽  
Mefkure Eraslan Sahin ◽  
Yusuf Madendag ◽  
Erdem Sahin ◽  
Cigdem Karakukcu
Keyword(s):  
Protease Inhibitor ◽  
Secretory Leukocyte Protease Inhibitor ◽  
Unexplained Infertility ◽  
Cervical Mucus

scholarly journals SLPI is a critical mediator that controls PTH-induced bone formation

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Akito Morimoto ◽  
Junichi Kikuta ◽  
Keizo Nishikawa ◽  
Takao Sudo ◽  
Maki Uenaka ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Bone Resorption ◽  
Bone Formation ◽  
Protease Inhibitor ◽  
Bone Metabolism ◽  
Serine Protease ◽  
Serine Protease Inhibitor ◽  
Secretory Leukocyte Protease Inhibitor ◽  
Bone Imaging ◽  
Genetic Ablation

AbstractOsteoclastic bone resorption and osteoblastic bone formation/replenishment are closely coupled in bone metabolism. Anabolic parathyroid hormone (PTH), which is commonly used for treating osteoporosis, shifts the balance from osteoclastic to osteoblastic, although it is unclear how these cells are coordinately regulated by PTH. Here, we identify a serine protease inhibitor, secretory leukocyte protease inhibitor (SLPI), as a critical mediator that is involved in the PTH-mediated shift to the osteoblastic phase. Slpi is highly upregulated in osteoblasts by PTH, while genetic ablation of Slpi severely impairs PTH-induced bone formation. Slpi induction in osteoblasts enhances its differentiation, and increases osteoblast–osteoclast contact, thereby suppressing osteoclastic function. Intravital bone imaging reveals that the PTH-mediated association between osteoblasts and osteoclasts is disrupted in the absence of SLPI. Collectively, these results demonstrate that SLPI regulates the communication between osteoblasts and osteoclasts to promote PTH-induced bone anabolism.

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