scholarly journals Specificity of aminergic status in skin and tumor of C57BL/6-PlautmI.IBug-This Plau6FDhu/GFDhu mice with B16/F10 melanoma

2020 ◽  
Vol 66 (6) ◽  
pp. 707-711
Author(s):  
Oleg Kit ◽  
Elena Frantsiyants ◽  
Irina Kaplieva ◽  
Ekaterina Surikova ◽  
Irina Neskubina ◽  
...  
Keyword(s):  
Biogenic Amines ◽  
Knockout Mice ◽  
Gene Knockout ◽  
Local Stress ◽  
Plasminogen Activation ◽  
Intact Skin ◽  
Gene Knockout Mice ◽  
Hydroxyindoleacetic Acid ◽  
Solitary Metastases ◽  
Deficient Mice

Background. Systems of plasminogen activation and biogenic amines are involved in carcinogenesis, but their relationship has not been established. Aim – study of the quantitative specificity of biogenic amines in the skin and melanoma in urokinase-gene knockout mice. Materials and methods.  Levels of catecholamines, histamine, serotonin and 5-hydroxyindoleacetic acid (HIAA) were determined by ELISA in the skin and В16/F10 melanoma of urokinase (uPA) -gene knockout mice of both genders (n=24); С57ВL/6 mice (n=64) were controls (C). Results. Differential characteristics of melanoma development in uPA-deficient mice included: an earlier onset of the primary tumor and its slow growth, more pronounced in females, in combination with hemorrhages in the lungs of males and solitary metastases in the lungs of females. This was facilitated by higher levels of norepinephrine in the skin of males/females – by 4.8/4.9 times, histamine – by 3.6/1.7 (p<0.05) times and serotonin – by 3.4/8.3 times. Dopamine accumulated in melanoma in all uPA-gene knockout mice: in females –1.6 times (p<0.05), in males – 2.1 times higher than in intact skin, with a 2.5 times reduction of norepinephrine in females. Levels of histamine decreased, but exceeded controls: in females – by 1.8 times (p<0.05), in males –by 3.5 times. Levels of serotonin in uPA-deficient females were as high, while in males they were 3.4 times lower than in intact skin. Conclusions. The specificity of the aminergic system in the skin of uPA-gene knockout mice demonstrated the inhibition of local stress and contributed to the reduction of malignant potential of melanoma by increasing immune properties of the skin.

scholarly journals Caspase-3/NLRP3 signaling in the mesenchymal stromal niche regulates myeloid-biased hematopoiesis

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Jing Zhang ◽  
Yaozhen Chen ◽  
Dandan Yin ◽  
Fan Feng ◽  
Qunxing An ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Knockout Mice ◽  
Caspase 3 ◽  
Ex Vivo ◽  
Gene Knockout ◽  
Hematopoietic Stem ◽  
Nlrp3 Gene ◽  
Gene Knockout Mice ◽  
Deficient Mice

Abstract Background The fate of hematopoietic stem cells (HSCs) is determined by a complex regulatory network that includes both intrinsic and extrinsic signals. In the past decades, many intrinsic key molecules of HSCs have been shown to control hematopoiesis homeostasis. Non-hematopoietic niche cells also contribute to the self-renewal, quiescence, and differentiation of HSCs. Mesenchymal stromal cells (MSCs) have been identified as important components of the niche. However, the regulatory role of MSCs in hematopoiesis has not been fully understood. Methods Caspase-3 and NLRP3 gene knockout mice were generated respectively, and hematopoietic development was evaluated in the peripheral circulation and bone marrow by flow cytometry, colony formation assay, and bone marrow transplantation. Bone-associated MSCs (BA-MSCs) were then isolated from gene knockout mice, and the effect of Caspase-3/NLRP3 deficient BA-MSCs on hematopoiesis regulation was explored in vivo and ex vivo. Results We report that Caspase-3 deficient mice exhibit increased myelopoiesis and an aberrant HSC pool. Ablation of Caspase-3 in BA-MSCs regulates myeloid lineage expansion by altering the expression of hematopoietic retention cytokines, including SCF and CXCL12. Interestingly, NLRP3 gene knockout mice share phenotypic similarities with Caspase-3 deficient mice. Additionally, we found that NLRP3 may play a role in myeloid development by affecting the cell cycle and apoptosis of hematopoietic progenitors. Conclusions Our data demonstrate that the Caspase-3/NLRP3 signaling functions as an important regulator in physiological hematopoiesis, which provides new insights regarding niche signals that influence hematopoiesis regulation in the bone marrow.

scholarly journals Comparison of Ocular Pathologies in Vitamin A–Deficient Mice and RPE65 Gene Knockout Mice

2011 ◽  
Vol 52 (8) ◽  
pp. 5507 ◽  
Author(s):  
Yang Hu ◽  
Ying Chen ◽  
Gennadiy Moiseyev ◽  
Yusuke Takahashi ◽  
Robert Mott ◽  
...  
Keyword(s):  
Vitamin A ◽  
Knockout Mice ◽  
Gene Knockout ◽  
Gene Knockout Mice ◽  
Deficient Mice

Detrimental implication of B1 receptors in myocardial ischemia: evidence from pharmacological blockade and gene knockout mice

2002 ◽  
Vol 2 (6) ◽  
pp. 815-822 ◽  
Author(s):  
Caroline Lagneux ◽  
Michael Bader ◽  
João B. Pesquero ◽  
Pierre Demenge ◽  
Christophe Ribuot
Keyword(s):  
Myocardial Ischemia ◽  
Knockout Mice ◽  
Gene Knockout ◽  
B1 Receptors ◽  
Gene Knockout Mice ◽  
Pharmacological Blockade

Enhanced antinociceptive effects of morphine in histamine H2 receptor gene knockout mice

2006 ◽  
Vol 51 (3) ◽  
pp. 612-622 ◽  
Author(s):  
Jalal Izadi Mobarakeh ◽  
Kazuhiro Takahashi ◽  
Shinobu Sakurada ◽  
Atsuo Kuramasu ◽  
Kazuhiko Yanai
Keyword(s):  
Knockout Mice ◽  
Gene Knockout ◽  
Receptor Gene ◽  
Histamine H2 Receptor ◽  
H2 Receptor ◽  
Antinociceptive Effects ◽  
Gene Knockout Mice

scholarly journals Increased glycosphingolipid levels in serum and aortae of apolipoprotein E gene knockout mice

2002 ◽  
Vol 43 (2) ◽  
pp. 205-214 ◽  
Author(s):  
Brett Garner ◽  
David A. Priestman ◽  
Roland Stocker ◽  
David J. Harvey ◽  
Terry D. Butters ◽  
...  
Keyword(s):  
Apolipoprotein E ◽  
Knockout Mice ◽  
Gene Knockout ◽  
E Gene ◽  
Apolipoprotein E Gene ◽  
Gene Knockout Mice

scholarly journals The Alopecia Areata Phenotype Is Induced by the Water Avoidance Stress Test In cchcr1-Deficient Mice

Biomedicines ◽  
2021 ◽  
Vol 9 (7) ◽  
pp. 840
Author(s):  
Qiaofeng Zhao ◽  
Satoshi Koyama ◽  
Nagisa Yoshihara ◽  
Atsushi Takagi ◽  
Etsuko Komiyama ◽  
...  
Keyword(s):  
Alopecia Areata ◽  
Gene Knockout ◽  
Stress Test ◽  
Coiled Coil ◽  
Risk Haplotype ◽  
Gene Expression Microarray ◽  
Wild Type ◽  
Gene Knockout Mice ◽  
Deficient Mice ◽  
Gene Expression Microarray Analysis

We recently discovered a nonsynonymous variant in the coiled-coil alpha-helical rod protein 1 (CCHCR1) gene within the alopecia areata (AA) risk haplotype. We also reported that the engineered mice with this risk allele exhibited. To investigate more about the involvement of the CCHCR1 gene in AA pathogenesis, we developed an AA model using C57BL/6N cchcr1 gene knockout mice. In this study, mice (6–8 weeks) were divided into two groups: cchcr1−/− mice and wild-type (WT) littermates. Both groups were subjected to a water avoidance stress (WAS) test. Eight weeks after the WAS test, 25% of cchcr1−/− mice exhibited non-inflammatory foci of alopecia on the dorsal skin. On the other hand, none of wild-type littermates cause hair loss. The foci resembled human AA in terms of gross morphology, trichoscopic findings and histological findings. Additionally, gene expression microarray analysis of cchcr1−/− mice revealed abnormalities of hair related genes compared to the control. Our results strongly suggest that CCHCR1 is associated with AA pathogenesis and that cchcr1−/− mice are a good model for investigating AA.

Serotonin2A/C receptors mediate the aggressive phenotype of TLX gene knockout mice

2013 ◽  
Vol 256 ◽  
pp. 354-361 ◽  
Author(s):  
Pablo Juárez ◽  
Maria G. Valdovinos ◽  
Michael E. May ◽  
Blair P. Lloyd ◽  
Maria H. Couppis ◽  
...  
Keyword(s):  
Knockout Mice ◽  
Gene Knockout ◽  
Aggressive Phenotype ◽  
Gene Knockout Mice

scholarly journals Age-Dependent Defects of Regulatory B Cells in Wiskott-Aldrich Syndrome Gene Knockout Mice

PLoS ONE ◽  
2015 ◽  
Vol 10 (10) ◽  
pp. e0139729 ◽  
Author(s):  
Tadafumi Yokoyama ◽  
Ayumi Yoshizaki ◽  
Karen L. Simon ◽  
Martha R. Kirby ◽  
Stacie M. Anderson ◽  
...  
Keyword(s):  
B Cells ◽  
Knockout Mice ◽  
Gene Knockout ◽  
Regulatory B Cells ◽  
Wiskott Aldrich Syndrome ◽  
Age Dependent ◽  
Gene Knockout Mice
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