scholarly journals Delta opioid receptors on nociceptive sensory neurons mediate peripheral endogenous analgesia in colitis

2022 ◽  
Vol 19 (1) ◽  
Author(s):  
Xavier Mas-Orea ◽  
Lilian Basso ◽  
Catherine Blanpied ◽  
Claire Gaveriaux-Ruff ◽  
Nicolas Cenac ◽  
...  
Keyword(s):  
T Lymphocytes ◽  
Sensory Neurons ◽  
Opioid Receptors ◽  
Knockout Mice ◽  
Colonic Mucosa ◽  
Visceral Pain ◽  
Conditional Knockout ◽  
Sensory Nerves ◽  
Conditional Knockout Mice ◽  
Endogenous Analgesia

Abstract Background Inflammatory visceral pain is endogenously controlled by enkephalins locally released by mucosal CD4+ T lymphocytes in mice. The present study aimed at identifying opioid receptor(s) expressed on nociceptive sensory nerves involved in this peripheral opioid-mediated analgesia. Methods The peripheral analgesia associated with the accumulation of CD4+ T lymphocytes within the inflamed colonic mucosa was assessed in conditional knockout mice specifically deleted for either of the two opioid receptors for enkephalins (i.e., µ (MOR) and δ (DOR) receptors) in Nav1.8-expressing sensory neurons in the dextran sulfate sodium (DSS)-induced colitis model. Results Endogenous analgesia is lost in conditional knockout mice for DOR, but not MOR at the later phase of the DSS-induced colitis. The absence of either of the opioid receptors on sensory nerves had no impact on both the colitis severity and the rate of T lymphocytes infiltrating the inflamed colonic mucosa. Conclusion The key role of DOR on primary afferents in relieving intestinal inflammatory pain opens new therapeutic opportunities for peripherally restricted DOR analgesics to avoid most of the side effects associated with MOR-targeting drugs used in intestinal disorders.

scholarly journals Mu Opioid Receptors on Primary Afferent Nav1.8 Neurons Contribute to Opiate-Induced Analgesia: Insight from Conditional Knockout Mice

PLoS ONE ◽  
2013 ◽  
Vol 8 (9) ◽  
pp. e74706 ◽  
Author(s):  
Raphaël Weibel ◽  
David Reiss ◽  
Laurie Karchewski ◽  
Olivier Gardon ◽  
Audrey Matifas ◽  
...  
Keyword(s):  
Opioid Receptors ◽  
Knockout Mice ◽  
Conditional Knockout ◽  
Mu Opioid Receptors ◽  
Primary Afferent ◽  
Mu Opioid ◽  
Conditional Knockout Mice

Ankyrin-G heterozygous conditional knockout mice display increased sensitivity to social defeat stress

2021 ◽  
Author(s):  
Zachary A. Cordner ◽  
Seva G. Khambadkone ◽  
Shanshan Zhu ◽  
Justin Bai ◽  
Rasadokht Forati ◽  
...  
Keyword(s):  
Knockout Mice ◽  
Social Defeat ◽  
Conditional Knockout ◽  
Social Defeat Stress ◽  
Conditional Knockout Mice ◽  
Ankyrin G ◽  
Increased Sensitivity

Reduced hippocampal ten-eleven translocation 3 (Tet3) protein expression in Tet3 conditional knockout mice

2021 ◽  
Vol 26 (5) ◽  
pp. 1425-1425
Author(s):  
Cláudia Antunes ◽  
Jorge D. Da Silva ◽  
Sónia Guerra-Gomes ◽  
Nuno D. Alves ◽  
Fábio Ferreira ◽  
...  
Keyword(s):  
Protein Expression ◽  
Knockout Mice ◽  
Conditional Knockout ◽  
Conditional Knockout Mice

scholarly journals Ultrastructural pathological changes in the cochlear cells of connexin 26 conditional knockout mice

2013 ◽  
Vol 8 (4) ◽  
pp. 1029-1036 ◽  
Author(s):  
LAN LIN ◽  
YUN-FENG WANG ◽  
SHU-YI WANG ◽  
SHAO-FENG LIU ◽  
ZHANG YU ◽  
...  
Keyword(s):  
Knockout Mice ◽  
Conditional Knockout ◽  
Connexin 26 ◽  
Pathological Changes ◽  
Conditional Knockout Mice

scholarly journals Endothelial cells produce bone morphogenetic protein 6 required for iron homeostasis in mice

Blood ◽  
2017 ◽  
Vol 129 (4) ◽  
pp. 405-414 ◽  
Author(s):  
Susanna Canali ◽  
Kimberly B. Zumbrennen-Bullough ◽  
Amanda B. Core ◽  
Chia-Yu Wang ◽  
Manfred Nairz ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Bone Morphogenetic Protein ◽  
Knockout Mice ◽  
Iron Homeostasis ◽  
Conditional Knockout ◽  
Conditional Knockout Mice ◽  
Morphogenetic Protein ◽  
Key Points ◽  
Paracrine Actions ◽  
Bone Morphogenetic Protein 6

Key Points Endothelial Bmp6 conditional knockout mice exhibit hemochromatosis, whereas hepatocyte and macrophage Bmp6 conditional knockout mice do not. Our data support a model in which EC Bmp6 has paracrine actions on hepatocyte hemojuvelin to regulate hepcidin production.

scholarly journals Epithelial (E)-Cadherin is a Novel Mediator of Platelet Aggregation and Clot Stability

2019 ◽  
Vol 119 (05) ◽  
pp. 744-757 ◽  
Author(s):  
Vanessa Scanlon ◽  
Alexandra Teixeira ◽  
Tarun Tyagi ◽  
Siying Zou ◽  
Ping-Xia Zhang ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Knockout Mice ◽  
Glycogen Synthase ◽  
Conditional Knockout ◽  
Platelet Production ◽  
Conditional Knockout Mice ◽  
Clot Stability ◽  
E Cadherin

AbstractCadherins play a major role in mediating cell–cell adhesion, which shares many parallels with platelet–platelet interactions during aggregate formation and clot stabilization. Platelets express epithelial (E)-cadherin, but its contribution to platelet function and/or platelet production is currently unknown. To assess the role of E-cadherin in platelet production and function in vitro and in vivo, we utilized a megakaryocyte-specific E-cadherin knockout mouse model. Loss of E-cadherin in megakaryocytes does not affect megakaryocyte maturation, platelet number or size. However, platelet dysfunction in the absence of E-cadherin is revealed when conditional knockout mice are challenged with acute antibody-mediated platelet depletion. Unlike wild-type mice that recover fully, knockout mice die within 72 hours post-antibody administration, likely from haemorrhage. Furthermore, conditional knockout mice have prolonged tail bleeding times, unstable clot formation, reduced clot retraction and reduced fibrin deposition in in vivo injury models. Murine platelet aggregation in vitro in response to thrombin and thrombin receptor activating peptide is compromised in E-cadherin null platelets, while aggregation in response to adenosine diphosphate (ADP) is not significantly different. Consistent with this, in vitro aggregation of primary human platelets in response to thrombin is decreased by an inhibitory E-cadherin antibody. Integrin activation and granule secretion in response to ADP and thrombin are not affected in E-cadherin null platelets, but Akt and glycogen synthase kinase 3β (GSK3β) activation are attenuated, suggesting a that E-cadherin contributes to aggregation, clot stabilization and retraction that is mediated by phosphoinositide 3-kinase/Akt/GSK3β signalling. In summary, E-cadherin plays a salient role in platelet aggregation and clot stability.

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