Effect of citronellol on NF‐kB inflammatory signaling molecules in chemical carcinogen‐induced mammary cancer in the rat model

2020 ◽  
Vol 34 (3) ◽  
Author(s):  
Rajendran Jayaganesh ◽  
Pachaiappan Pugalendhi ◽  
Raju Murali
Keyword(s):  
Rat Model ◽  
Mammary Cancer ◽  
Signaling Molecules ◽  
Chemical Carcinogen ◽  
Inflammatory Signaling

scholarly journals Microglia, Cytokines, and Neural Activity: Unexpected Interactions in Brain Development and Function

2021 ◽  
Vol 12 ◽  
Author(s):  
Austin Ferro ◽  
Yohan S. S. Auguste ◽  
Lucas Cheadle
Keyword(s):  
Brain Development ◽  
Signaling Pathways ◽  
Immune Cells ◽  
Neural Activity ◽  
Signaling Molecules ◽  
Evolutionary Strategy ◽  
Inflammatory Signaling ◽  
Peripheral Tissues ◽  
And Function ◽  
The Brain

Intercellular signaling molecules such as cytokines and their receptors enable immune cells to communicate with one another and their surrounding microenvironments. Emerging evidence suggests that the same signaling pathways that regulate inflammatory responses to injury and disease outside of the brain also play powerful roles in brain development, plasticity, and function. These observations raise the question of how the same signaling molecules can play such distinct roles in peripheral tissues compared to the central nervous system, a system previously thought to be largely protected from inflammatory signaling. Here, we review evidence that the specialized roles of immune signaling molecules such as cytokines in the brain are to a large extent shaped by neural activity, a key feature of the brain that reflects active communication between neurons at synapses. We discuss the known mechanisms through which microglia, the resident immune cells of the brain, respond to increases and decreases in activity by engaging classical inflammatory signaling cascades to assemble, remodel, and eliminate synapses across the lifespan. We integrate evidence from (1) in vivo imaging studies of microglia-neuron interactions, (2) developmental studies across multiple neural circuits, and (3) molecular studies of activity-dependent gene expression in microglia and neurons to highlight the specific roles of activity in defining immune pathway function in the brain. Given that the repurposing of signaling pathways across different tissues may be an important evolutionary strategy to overcome the limited size of the genome, understanding how cytokine function is established and maintained in the brain could lead to key insights into neurological health and disease.

scholarly journals Rat Model of Bone Metastasis Obtained by Mammary Cancer Transplantation

1993 ◽  
Vol 2 (2) ◽  
pp. 193-198,169 ◽  
Author(s):  
Akishige Ohta ◽  
Takashi Matsubayashi ◽  
Hitoshi Takahara ◽  
Mineko Uemae ◽  
Shigenobu Nakayama
Keyword(s):  
Bone Metastasis ◽  
Rat Model ◽  
Mammary Cancer

Cardiovascular expression of inflammatory signaling molecules, the kinin B1 receptor and COX2, in the rabbit: Effects of LPS, anti-inflammatory and anti-hypertensive drugs

2008 ◽  
Vol 146 (1-3) ◽  
pp. 157-168 ◽  
Author(s):  
Marie-Thérèse Bawolak ◽  
Karine Touzin ◽  
Marie Eve Moreau ◽  
Anik Désormeaux ◽  
Albert Adam ◽  
...  
Keyword(s):  
Signaling Molecules ◽  
Inflammatory Signaling ◽  
B1 Receptor ◽  
Kinin B1 Receptor ◽  
Anti Inflammatory

scholarly journals A Comparative Approach of Tumor-Associated Inflammation in Mammary Cancer between Humans and Dogs

2016 ◽  
Vol 2016 ◽  
pp. 1-12 ◽  
Author(s):  
Maria Isabel Carvalho ◽  
Ricardo Silva-Carvalho ◽  
Isabel Pires ◽  
Justina Prada ◽  
Rodolfo Bianchini ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Immune Cells ◽  
Mammary Cancer ◽  
Inflammatory Cells ◽  
Mammary Carcinogenesis ◽  
Signaling Molecules ◽  
Comparative Approach ◽  
Human Breast ◽  
Infiltrating Cells ◽  
Inflammatory State

Infiltrating cells of the immune system are widely accepted to be generic constituents of tumor microenvironment. It has been well established that the development of mammary cancer, both in humans and in dogs, is associated with alterations in numbers and functions of immune cells at the sites of tumor progression. These tumor infiltrating immune cells seem to exhibit exclusive phenotypic and functional characteristics and mammary cancer cells can take advantage of signaling molecules released by them. Cancer related inflammation has an important role in mammary carcinogenesis, contributing to the acquisition of core hallmark capabilities that allow cancer cells to survive, proliferate, and disseminate. Indeed, recent studies in human breast cancer and in canine mammary tumors have identified a growing list of signaling molecules released by inflammatory cells that serve as effectors of their tumor-promoting actions. These include the COX-2, the tumor EGF, the angiogenic VEGF, other proangiogenic factors, and a large variety of chemokines and cytokines that amplify the inflammatory state. This review describes the intertwined signaling pathways shared by T-lymphocytic/macrophage infiltrates and important tissue biomarkers in both human and dog mammary carcinogenesis.

Breaking the cycle: the role of omega-3 polyunsaturated fatty acids in inflammation-driven cancers

2014 ◽  
Vol 92 (5) ◽  
pp. 321-328 ◽  
Author(s):  
William L. Patterson ◽  
Philippe T. Georgel
Keyword(s):  
Fatty Acids ◽  
Transcription Factors ◽  
Polyunsaturated Fatty Acids ◽  
Chronic Inflammation ◽  
Cancer Progression ◽  
Immune Cells ◽  
Signaling Molecules ◽  
Inflammatory Signaling ◽  
Vast Number ◽  
Anti Inflammatory

Chronic inflammation is a cyclical, self-stimulating process. Immune cells called to sites of inflammation release pro-inflammatory signaling molecules that stimulate activation of inducible enzymes and transcription factors. These enzymes and transcription factors then stimulate production of signaling molecules that attract more immune cells and induce more enzymatic and transcriptional activity, creating a perpetual loop of inflammation. This self-renewing pool of inflammatory stimuli makes for an ideal tumor microenvironment, and chronic inflammation has been linked to oncogenesis, tumor growth, tumor cell survival, and metastasis. Three protein pathways in particular, nuclear factor kappa B (NF-kB), cyclooxygenase (COX), and lipoxygenase (LOX), provide excellent examples of the cyclical, self-renewing nature of chronic inflammation-driven cancers. NF-kB is an inducible transcription factor responsible for the expression of a vast number of inflammation and cancer related genes. COX and LOX convert omega-6 (n-6) and omga-3 (n-3) polyunsaturated fatty acids (PUFA) into pro- and anti-inflammatory signaling molecules. These signaling molecules stimulate or repress activity of all three of these pathways. In this review, we will discuss the pro- and anti-inflammatory functions of these fatty acids and their role in chronic inflammation and cancer progression.

scholarly journals No effect of a high-fat diet on promotion of sex hormone-induced prostate and mammary carcinogenesis in the Noble rat model

2002 ◽  
Vol 88 (4) ◽  
pp. 399-409 ◽  
Author(s):  
G. Leung ◽  
I. F. F. Benzie ◽  
A. Cheung ◽  
S. W. Tsao ◽  
Y. C. Wong
Keyword(s):  
Weight Gain ◽  
Rat Model ◽  
Dietary Fat ◽  
High Fat Diet ◽  
Mammary Cancer ◽  
Mammary Carcinogenesis ◽  
Sex Hormone ◽  
Female Rats ◽  
Male Rats ◽  
High Fat

Results of international correlation and migrant studies suggest that dietary fat promotes carcinogenesis in hormone-sensitive sites, but this is disputed. In the present study, we used a Noble rat model of sex hormone-induced cancers to examine the effect of a high-fat diet on the incidence and latency of prostate and mammary cancer in male (n 139) and female (n 72) animals respectively. We also measured α-tocopherol levels in female breast tissue to determine whether a high intake of polyunsaturated fatty acids depletes antioxidant defence in target tissues, providing a possible potentiating mechanism for carcinogenesis. Results showed a very high incidence of hormone-induced adenocarcinomas of prostate and mammary gland, irrespective of diet. There was no difference in the pattern of carcinogenesis in different prostatic locations, weight of the prostate, or weight gain between male rats on the high-fat diet compared with the control (standard, low-fat) diet. In female rats, the incidence of mammary cancer and the body-weight gain were the same in both dietary groups, and breast α-tocopherol was also unaffected by dietary fat intake. Our present results are supportive of recent cohort studies that reported no significant association between intake of fat and the development of human prostate and breast cancer, and do not support a role for dietary fat in promoting sex hormone-induced prostate and mammary carcinogenesis.

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