Sense-and-Respond Strategies Survey

Hypoxia—reduction in oxygen availability—plays key roles in both physiological and pathological processes. Given the importance of oxygen for cell and organism viability, mechanisms to sense and respond to hypoxia are in place. A variety of enzymes utilise molecular oxygen, but of particular importance to oxygen sensing are the 2-oxoglutarate (2-OG) dependent dioxygenases (2-OGDs). Of these, Prolyl-hydroxylases have long been recognised to control the levels and function of Hypoxia Inducible Factor (HIF), a master transcriptional regulator in hypoxia, via their hydroxylase activity. However, recent studies are revealing that dioxygenases are involved in almost all aspects of gene regulation, including chromatin organisation, transcription and translation. We highlight the relevance of HIF and 2-OGDs in the control of gene expression in response to hypoxia and their relevance to human biology and health.

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Zelluläres Tauziehen: Wie Zellen auf mechanischen Stress antworten

BIOspektrum ◽

10.1007/s12268-021-1598-0 ◽

2021 ◽

Vol 27 (4) ◽

pp. 385-389

Author(s):

Kai Weissenbruch ◽

Marc Hippler ◽

Martin Bastmeyer

Keyword(s):

Tissue Homeostasis ◽

Physical Basis ◽

Technical Advance ◽

Molecular Scale ◽

Sense And Respond ◽

Intracellular Forces

AbstractThe ability of cells to sense and respond to extracellular forces is critical for cellular and tissue homeostasis. Tension or compression act on our body ubiquitously and cells respond to such mechanical cues by producing intracellular forces on their own. In this article, we briefly highlight the cellular and physical basis driving these phenomena and discuss our recent technical advance to stimulate and monitor the cellular mechanoresponse on a molecular scale.

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Combinatorial Control of Gene Expression

BioMed Research International ◽

10.1155/2013/407263 ◽

2013 ◽

Vol 2013 ◽

pp. 1-11 ◽

Cited By ~ 18

Author(s):

Soumya Bhattacharjee ◽

Kaushik Renganaath ◽

Rajesh Mehrotra ◽

Sandhya Mehrotra

Keyword(s):

Gene Expression ◽

Short Description ◽

Controlling Factors ◽

Environmental Cues ◽

Control Of Gene Expression ◽

Environmental Signals ◽

Combinatorial Control ◽

Sense And Respond ◽

Eukaryotic Organisms

The complexity and diversity of eukaryotic organisms are a feat of nature’s engineering. Pulling the strings of such an intricate machinery requires an even more masterful and crafty approach. Only the number and type of responses that they generate exceed the staggering proportions of environmental signals perceived and processed by eukaryotes. Hence, at first glance, the cell’s sparse stockpile of controlling factors does not seem remotely adequate to carry out this response. The question as to how eukaryotes sense and respond to environmental cues has no single answer. It is an amalgamation, an interplay between several processes, pathways, and factors—a combinatorial control. A short description of some of the most important elements that operate this entire conglomerate is given in this paper.

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Coupling between apical tension and basal adhesion allow epithelia to collectively sense and respond to substrate topography over long distances

Integrative Biology ◽

10.1039/c5ib00240k ◽

2015 ◽

Vol 7 (12) ◽

pp. 1611-1621 ◽

Cited By ~ 16

Author(s):

Kyle E. Broaders ◽

Alec E. Cerchiari ◽

Zev J. Gartner

Keyword(s):

Substrate Topography ◽

Cell Substrate ◽

Sense And Respond ◽

Cell Medium ◽

Cell Cell

Epithelia have the capacity to sense and respond to substrate topography through the coupling of tensions at the cell–cell, cell–substrate, and cell–medium interfaces.

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The capacity of Aspergillus niger to sense and respond to cell wall stress requires at least three transcription factors: RlmA, MsnA and CrzA

Fungal Biology and Biotechnology ◽

10.1186/s40694-014-0005-8 ◽

2014 ◽

Vol 1 (1) ◽

Cited By ~ 6

Author(s):

Markus RM Fiedler ◽

Annett Lorenz ◽

Benjamin M Nitsche ◽

Cees AMJJ van den Hondel ◽

Arthur FJ Ram ◽

...

Keyword(s):

Cell Wall ◽

Transcription Factors ◽

Aspergillus Niger ◽

Wall Stress ◽

Cell Wall Stress ◽

Sense And Respond

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Functional Mapping of YadA- and Ail-Mediated Binding of Human Factor H to Yersinia enterocolitica Serotype O:3

Infection and Immunity ◽

10.1128/iai.00314-08 ◽

2008 ◽

Vol 76 (11) ◽

pp. 5016-5027 ◽

Cited By ~ 45

Author(s):

Marta Biedzka-Sarek ◽

Saara Salmenlinna ◽

Markus Gruber ◽

Andrei N. Lupas ◽

Seppo Meri ◽

...

Keyword(s):

Yersinia Enterocolitica ◽

Alternative Pathway ◽

Outer Membrane Proteins ◽

Factor H ◽

Complement Alternative Pathway ◽

Human Host ◽

Serotype O ◽

Complement Resistance ◽

Sense And Respond ◽

Active Complement

ABSTRACT Yersinia enterocolitica is an enteric pathogen that exploits diverse means to survive in the human host. Upon Y. enterocolitica entry into the human host, bacteria sense and respond to variety of signals, one of which is the temperature. Temperature in particular has a profound impact on Y. enterocolitica gene expression, as most of its virulence factors are expressed exclusively at 37°C. These include two outer membrane proteins, YadA and Ail, that function as adhesins and complement resistance (CR) factors. Both YadA and Ail bind the functionally active complement alternative pathway regulator factor H (FH). In this study, we characterized regions on both proteins involved in CR and the interaction with FH. Twenty-eight mutants having short (7 to 41 amino acids) internal deletions within the neck and stalk of YadA and two complement-sensitive site-directed Ail mutants were constructed to map the CR and FH binding regions of YadA and Ail. Functional analysis of the YadA mutants revealed that the stalk of YadA is required for both CR and FH binding and that FH appears to target several conformational and discontinuous sites of the YadA stalk. On the other hand, the complement-sensitive Ail mutants were not affected in FH binding. Our results also suggested that Ail- and YadA-mediated CR does not depend solely on FH binding.

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Abstract P415: ACE N-domain Regulates High-glucose Mediated Interleukin-1 beta Production by Renal Epithelial Cells Independently From Angiotensin II Generation

Hypertension ◽

10.1161/hyp.70.suppl_1.p415 ◽

2017 ◽

Vol 70 (suppl_1) ◽

Author(s):

Jorge F Giani ◽

Ellen A Bernstein ◽

Masahiro Eriguchi ◽

Romer A Gonzalez-Villalobos ◽

Kenneth E Bernstein

Keyword(s):

Diabetic Nephropathy ◽

Angiotensin Ii ◽

Epithelial Cells ◽

High Glucose ◽

Interleukin 1 ◽

Kidney Injury ◽

Fold Increase ◽

Renal Epithelial Cells ◽

Proximal Tubular ◽

Sense And Respond

Research studies demonstrated that interleukin (IL)-1β contributes to the development of diabetic nephropathy and hypertension. However, the origin and regulation of IL-1β synthesis during diabetic kidney injury are still unknown. Here, we hypothesize that renal epithelial cells produce IL-1β in response to a high glucose stress and that angiotensin converting enzyme (ACE) plays a key role in this process. To study this, we isolated proximal tubular (PT) epithelial cells from wild-type (WT) and mice lacking either the ACE N-domain (NKO) or the C-domain (CKO) catalytic activity. These cells were exposed to normal (5 mM) or high (30 mM) glucose for 24 hours. IL-1β produced by PT cells were assessed by ELISA and RT-PCR. High glucose induced WT PT cells to release significant amounts of IL-1β (from 5±1 to 70±6 pg/ml, p<0.001; n=6). When WT PT cells were exposed to a high glucose media in the presence of an ACE inhibitor (lisinopril, 10 mM), IL-1β levels were significantly reduced (from 70±6 to 38±6 pg/ml, p<0.01). In contrast, AT1 receptor blockade by losartan did not change the amount of IL-1β produced by WT PT cells. To determine which ACE domain is associated with IL-1β production, NKO and CKO PT cells were exposed to high glucose. Strikingly, NKO PT cells released lower amounts of IL-1β when exposed to high glucose compared to WT (NKO: 15±7 vs. WT: 79±9 pg/ml, p<0.01, n=4). No differences were observed between WT and CKO PT cells. Since the ACE N-domain degrades the anti-inflammatory tetrapeptide N-acetyl-Ser-Asp-Lys-Pro (AcSDKP), we tested whether the lower IL-1β production in NKO PT cells was due to an accumulation of AcSDKP. For this, we pre-treated NKO PT cells with a prolyl endopeptidase inhibitor (S17092, 50μM) to prevent the production of AcSDKP. Notably, this treatment increased the IL-1β response to high glucose in NKO PT cells (2.1±0.3-fold increase, p<0.01, n=4). Our data indicate that: 1) PT cells can sense and respond to high glucose by secreting IL-1β and 2) the absence of the ACE N-domain blunts the production of IL-1β through a mechanism that involves AcSDKP accumulation. In conclusion, ACE might contribute to the inflammatory response that underlays diabetic nephropathy independently from angiotensin II generation.

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β-Cell adaptation in 60% pancreatectomy rats that preserves normoinsulinemia and normoglycemia

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.2000.279.1.e68 ◽

2000 ◽

Vol 279 (1) ◽

pp. E68-E73 ◽

Cited By ~ 30

Author(s):

Ye Qi Liu ◽

Peter W. Nevin ◽

Jack L. Leahy

Keyword(s):

Insulin Secretion ◽

Regulatory Element ◽

Cell Mass ◽

Maximal Velocity ◽

Β Cells ◽

Β Cell ◽

Biochemical Basis ◽

Adaptive Mechanisms ◽

Sense And Respond ◽

Glucose Responsiveness

Islet β-cells are the regulatory element of the glucose homeostasis system. When functioning normally, they precisely counterbalance changes in insulin sensitivity or β-cell mass to preserve normoglycemia. This understanding seems counter to the dogma that β-cells are regulated by glycemia. We studied 60% pancreatectomy rats (Px) 4 wk postsurgery to elucidate the β-cell adaptive mechanisms. Nonfasting glycemia and insulinemia were identical in Px and sham-operated controls. There was partial regeneration of the excised β-cells in the Px rats, but it was limited in scope, with the pancreas β-cell mass reaching 55% of the shams (40% increase from the time of surgery). More consequential was a heightened glucose responsiveness of Px islets so that glucose utilization and insulin secretion per milligram of islet protein were both 80% augmented at normal levels of glycemia. Investigation of the biochemical basis showed a doubled glucokinase maximal velocity in Px islets, with no change in the glucokinase protein concentration after adjustment for the different β-cell mass in Px and sham islets. Hexokinase activity measured in islet extracts was also minimally increased, but the glucose 6-phosphate concentration and basal glucose usage of Px islets were not different from those in islets from sham-operated rats. The dominant β-cell adaptive response in the 60% Px rats was an increased catalytic activity of glucokinase. The remaining β-cells thus sense, and respond to, perceived hyperglycemia despite glycemia actually being normal. β-Cell mass and insulin secretion are both augmented so that whole pancreas insulin output, and consequently glycemia, are maintained at normal levels.

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Adaptive enterprise design: The sense‐and‐respond model

Planning Review ◽

10.1108/eb054506 ◽

1995 ◽

Vol 23 (3) ◽

pp. 6-42 ◽

Cited By ~ 21

Author(s):

Stephen H. Haeckel

Keyword(s):

Enterprise Design ◽

Sense And Respond

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The Mast Cell-Aryl Hydrocarbon Receptor Interplay at the Host-Microbe Interface

Mediators of Inflammation ◽

10.1155/2018/7396136 ◽

2018 ◽

Vol 2018 ◽

pp. 1-6

Author(s):

Claudio Costantini ◽

Giorgia Renga ◽

Vasilis Oikonomou ◽

Giuseppe Paolicelli ◽

Monica Borghi ◽

...

Keyword(s):

Mast Cell ◽

Mast Cells ◽

Aryl Hydrocarbon Receptor ◽

Current Knowledge ◽

Cell Physiology ◽

Effector Functions ◽

Host Protection ◽

Aryl Hydrocarbon ◽

Environmental Agents ◽

Sense And Respond

Mast cells are increasingly being recognized as crucial cells in the response of the organism to environmental agents. Interestingly, the ability of mast cells to sense and respond to external cues is modulated by the microenvironment that surrounds mast cells and influences their differentiation. The scenario that is emerging unveils a delicate equilibrium that balances the effector functions of mast cells to guarantee host protection without compromising tissue homeostasis. Among the environmental components able to mold mast cells and fine-tune their effector functions, the microorganisms that colonize the human body, collectively known as microbiome, certainly play a key role. Indeed, microorganisms can regulate not only the survival, recruitment, and maturation of mast cells but also their activity by setting the threshold required for the exploitation of their different effector functions. Herein, we summarize the current knowledge about the mechanisms underlying the ability of the microorganisms to regulate mast cell physiology and discuss potential deviations that result in pathological consequences. We will discuss the pivotal role of the aryl hydrocarbon receptor in sensing the environment and shaping mast cell adaptation at the host-microbe interface.

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