Jerrold R Turner

The University of Chicago Medical Center, Chicago, Illinois, United States

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Publications (181)1612.51 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Tight junctions create a paracellular barrier that is essential for survival of complex organisms. In many cases tight junctions define separate, generally sterile, tissue compartments. In the skin and gut, tight junctions must also seal the paracellular space to prevent microbiota from accessing the internal milieu. This is a relatively simple task in the integument, where an absolute barrier is effective. However, intestinal epithelial tight junctions are charged with the far more complex task of supporting paracellular transport of water, ions, and nutrients while providing a barrier to microbial translocation. The delicate nature of this balance, which is disrupted in disease, makes the intestine a unique organ in which to explore the complexities of tight junction permeability and barrier regulation. Here we review recent progress in understanding the molecular determinants of barrier function and events responsible for regulation, and dysregulation, of tight junction permeability.
    Seminars in Cell and Developmental Biology 09/2014; · 6.20 Impact Factor
  • Gastrointestinal Endoscopy 09/2014; 80(3):516–517. · 5.21 Impact Factor
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    ABSTRACT: Approximately half of all adult burn patients are intoxicated at the time of their injury and have worsened clinical outcomes compared to those without prior alcohol exposure. This study tested the hypothesis that intoxication alters the gut-liver axis leading to increased pulmonary inflammation mediated by burn-induced IL-6 in the liver. To this end, C57BL/6 mice were given 1.2 g/kg ethanol 30 minutes prior to a 15% total body surface area burn. To restore gut barrier function, a specific myosin light chain kinase inhibitor [membrane-permeant inhibitor of kinase (PIK)] was administered 30 minutes after injury which we have demonstrated to reduce bacterial translocation from the gut. Limiting bacterial translocation with PIK attenuated hepatic damage as measured by a 47% reduction in serum alanine aminotransferase (p<0.05) as well as a 33% reduction in hepatic IL-6 mRNA expression (p<0.05) compared to intoxicated burned mice without PIK. This mitigation of hepatic damage was associated with a 49% decline in pulmonary neutrophil infiltration (p<0.05) and decreased alveolar wall thickening compared to matched controls. These results were reproduced by prophylactically reducing the bacterial load in the intestines with oral antibiotics before intoxication and burn. Overall these data suggest the gut-liver axis is deranged when intoxication precedes burn and that limiting bacterial translocation in this setting attenuates hepatic damage and pulmonary inflammation.
    American journal of physiology. Gastrointestinal and liver physiology. 08/2014;
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    ABSTRACT: Previous studies have shown a correlation between pretransplant conditioning intensity, intestinal barrier loss, and graft-versus-host disease (GVHD) severity. However, because irradiation and other forms of pretransplant conditioning have pleiotropic effects, the precise role of intestinal barrier loss in GVHD pathogenesis remains unclear. We developed GVHD models that allowed us to isolate the specific contributions of distinct pretransplant variables. Intestinal damage was required for the induction of minor mismatch [major histocompatibility complex (MHC)-matched] GVHD, but was not necessary for major mismatch GVHD, demonstrating fundamental pathogenic distinctions between these forms of disease. Moreover, recipient natural killer (NK) cells prevented minor mismatch GVHD by limiting expansion and target organ infiltration of alloreactive T cells via a perforin-dependent mechanism, revealing an immunoregulatory function of MHC-matched recipient NK cells in GVHD. Minor mismatch GVHD required MyD88-mediated Toll-like receptor 4 (TLR4) signaling on donor cells, and intestinal damage could be bypassed by parenteral lipopolysaccharide (LPS) administration, indicating a critical role for the influx of bacterial components triggered by intestinal barrier loss. In all, the data demonstrate that pretransplant conditioning plays a dual role in promoting minor mismatch GVHD by both depleting recipient NK cells and inducing intestinal barrier loss.
    Science translational medicine 07/2014; 6(243):243ra87. · 10.76 Impact Factor
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    ABSTRACT: Abnormal bacterial adherence and internalization in enterocytes have been documented in Crohn disease, celiac disease, surgical stress, and intestinal obstruction and are associated with low-level interferon (IFN)-γ production. How commensals gain access to epithelial soma through densely packed microvilli rooted on the terminal web (TW) remains unclear. We investigated molecular and ultrastructural mechanisms of bacterial endocytosis, focusing on regulatory roles of IFN-γ and myosin light chain kinase (MLCK) in TW myosin phosphorylation and brush border fanning. Mouse intestines were sham operated on or obstructed for 6 hours by loop ligation with intraluminally administered ML-7 (a MLCK inhibitor) or Y27632 (a Rho-associated kinase inhibitor). After intestinal obstruction, epithelial endocytosis and extraintestinal translocation of bacteria were observed in the absence of tight junctional damage. Enhanced TW myosin light chain phosphorylation, arc formation, and brush border fanning coincided with intermicrovillous bacterial penetration, which were inhibited by ML-7 and neutralizing anti-IFN-γ but not Y27632. The phenomena were not seen in mice genetically deficient for long MLCK-210 or IFN-γ. Stimulation of human Caco-2BBe cells with IFN-γ caused MLCK-dependent TW arc formation and brush border fanning, which preceded caveolin-mediated bacterial internalization through cholesterol-rich lipid rafts. In conclusion, epithelial MLCK-activated brush border fanning by IFN-γ promotes adherence and internalization of normally noninvasive enteric bacteria. Transcytotic commensal penetration may contribute to initiation or relapse of chronic inflammation.
    The American journal of pathology. 06/2014;
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    Gastroenterology 05/2014; 146(5):S783-4. · 12.82 Impact Factor
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    ABSTRACT: Sterol Response Element Binding Protein 2 (SREBP2) transcription factor is a master regulator of cholesterol homeostasis. Treatment with statins, inhibitors of cholesterol synthesis, activates intestinal SREBP2, which may hinder their cholesterol-lowering effects. Overactivation of SREBP2 in mouse liver was shown to have no effect on plasma cholesterol. However, the influence of activating intestinal SREBP2 on plasma cholesterol is not known. We have generated a novel transgenic mouse model with intestine specific overexpression of active SREBP2 (ISR2) driven by villin promoter. ISR2 mice showed overexpression of active SREBP2 specifically in the intestine. Microarray analysis of jejunal RNA from ISR2 mice showed a significant increase in genes involved in fatty acid and cholesterol synthesis. Cholesterol and triglyceride (TG) in jejunum and liver (mg/g protein) were significantly increased in ISR2 vs wild type mice. Serum Cholesterol was significantly increased in VLDL and LDL fractions whereas the level of serum triglycerides was decreased in ISR2 vs wild type mice. In conclusion, activation of intestinal SREBP2 alone seems to be sufficient to increase plasma cholesterol, highlighting the essential role of intestine in maintaining cholesterol homeostasis in the body.
    PLoS ONE 01/2014; 9(1):e84221. · 3.53 Impact Factor
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    ABSTRACT: In vitro and in vivo studies have implicated occludin in regulation of paracellular macromolecular flux at steady-state and in response to tumor necrosis factor (TNF). To define the roles of occludin in these processes, intestinal epithelia with stable occludin knockdown were established. Knockdown monolayers had markedly enhanced tight junction permeability to large molecules that could be modeled by size-selective channels with radii of ∼62.5Å. TNF increased paracellular flux of large molecules in occludin-sufficient, but not occludin-deficient, monolayers. Complementation using full length or C-terminal OCEL domain-deficient EGFP-occludin showed that TNF-induced occludin endocytosis and barrier regulation both required the OCEL domain. Either TNF treatment or OCEL deletion accelerated EGFP-occludin fluorescent recovery, but TNF treatment did not affect behavior of EGFP- occludin(ΔOCEL). Further, the free OCEL domain prevented TNF-induced acceleration of occludin fluorescent recovery, occludin endocytosis, and barrier loss. OCEL mutated within a recently-proposed ZO-1 binding domain (K433) could not inhibit TNF effects, but OCEL mutated within the ZO-1 SH3-GuK binding region (K485/K488) remained functional. We conclude that OCEL-mediated occludin interactions are essential for limiting paracellular macromolecular flux. Moreover, our data implicate interactions mediated by the OCEL K433 region as an effector of TNF-induced barrier regulation.
    Molecular biology of the cell 08/2013; · 5.98 Impact Factor
  • Emily S Turner, Jerrold R Turner
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    ABSTRACT: See "Identification of molecular subtypes of gastric cancer with different responses to PI3-kinase inhibitors and 5-fluorouracil," by Lei Z, Tan IB, Das K, et al, on page 000. Q1 A denocarcinoma of the stomach remains a major public health issue. Although the incidence of this cancer in the United States has been falling, with only 21,600 new cases expected in 2013, 1 the prognosis for patients remains grim. Despite improvements in treat-ment approaches, 5-year survival remains at <30%. 1 In addition to the typically advanced stage of diagnosis for most gastric adenocarcinomas, these dismal survival sta-tistics reflect the lack of effective treatment options. Identifying specific signaling pathways in individual pa-tients might improve treatment outcomes, but only limited data are available. In this issue of GASTROENTER-OLOGY, Lei et al 2 describe 1 approach to overcoming this obstacle. Their results identify 3 molecular signatures of gastric adenocarcinoma (Table 1). Patient survival data indicate that one of these subtypes may best be treated using 5-fluorouracil. In vitro data also suggest that another subtype may be particularly sensitive to phos-phatidyl-inositol-3-kinase inhibitors. This study builds on previous mRNA analyses of gastric cancers by this group and others. 3–10 By combining 192 previously reported 9 and 56 new microarray expression profiles, Lei et al 2 created a database describing 248 Sin-gaporean primary gastric cancers. These were broken into 3 unique groups using hierarchical clustering with itera-tive feature selection. The 201 gastric cancers that best represented the 3 groups were used to develop classifica-tion algorithms. The algorithms were then validated using a separate set of 70 Australian primary gastric cancers. Thus, at least for gastric cancers arising in Singapore and Australia, subclassification into the 3 groups is reproducible. To better understand the biological significance of the distinct groups, Lei et al 2 examined the differentially expressed genes. The clusters were designated as mesen-chymal, to reflect expression of genes in the epithelial-mesenchymal transition pathway; proliferative, because growth promoting oncogenic pathways were activated; and metabolic, owing to expression of genes associated with metabolic pathways. Further analyses of each group showed that mesen-chymal tumors lost expression of E-cadherin, the epithe-lial cadherin isoform. Consistent with the frequent loss of E-cadherin expression in signet ring cell gastric cancers, nearly 60% of mesenchymal tumors were classified as Lauren's diffuse type (Figure 1A), and 70% had at least some features of diffuse gastric cancer. 11 Further, consis-tent with reports that diffuse gastric cancers tend to be hypermethylated, 12 mesenchymal tumors displayed genomic hypermethylation. Transforming growth factor-b, vascular endothelial growth factor, nuclear factor-kB, mammalian target of rapamycin, sonic hedgehog, and stem cancer stem cell pathways were also activated in mesenchymal gastric cancers. In contrast, p53 mutations and DNA copy number variations were limited. In contrast with mesenchymal gastric adenocarcinomas, nearly 75% of proliferative tumors were Lauren's intestinal type (Figure 1B). These tumors tended to have activation of E2F, MYC, and RAS pathways and mutations of CCNE1, MYC, ERBB2, and KRAS. Proliferative cancers were hypomethylated and often harbored p53 mutations. These characteristics suggest that the proliferative cluster over-laps with Lauren's intestinal type and that this group includes tumors responsive to therapies targeting endo-thelial growth factor receptor (EGFR) Q2
    Gastroenterology 07/2013; · 12.82 Impact Factor
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    ABSTRACT: An association between inflammatory activity and colorectal neoplasia (CRN) has been documented in patients with ulcerative colitis (UC). However, previous studies did not address the duration of inflammation or the effects of therapy on risk for CRN. We investigated the effects of inflammation, therapies, and characteristics of patients with UC on their risk for CRN. We collected data from 141 patients with UC without CRN (controls), and 59 matched patients with UC who developed CRN (cases), comparing disease extent and duration and patients' ages. We used a new 6-point histologic inflammatory activity (HIA) scale to score biopsy fragments (n=4449). Information on medications, smoking status, primary sclerosing cholangitis (PSC), and family history of CRN were collected from the University of Chicago Inflammatory Bowel Disease Endoscopy Database. Relationships between HIA, clinical features, and CRN were assessed by conditional logistic regression. Cases and controls were similar in numbers of procedures and biopsies, exposure to steroids or mesalamine, smoking status, and family history of CRN. They differed in proportion of men vs women, exposure to immune modulators, and PSC prevalence. In univariate analysis, HIA was positively associated with CRN (odds ratio [OR], 2.56/ per unit increase; P=.001), whereas immune modulators (including azathioprine, 6-mercaptopurine, and methotrexate) reduced the risk for CRN (OR, 0.35; P<.01). HIA was also associated with CRN in multivariate analysis (OR, 3.68; P=.001). In a case-control study, we associated increased inflammation with CRN in patients with UC. Use of immune modulators reduced the risk for CRN, indicating that these drugs have chemoprotective effects. Based on these data, we propose new stratified surveillance and treatment strategies to prevent and detect CRN in patients with UC.
    Clinical gastroenterology and hepatology: the official clinical practice journal of the American Gastroenterological Association 07/2013; · 5.64 Impact Factor
  • Matthew A Odenwald, Jerrold R Turner
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    ABSTRACT: An essential role of the intestinal epithelium is to separate luminal contents from the interstitium, a function primarily determined by the integrity of the epithelium and the tight junction that seals the paracellular space. Intestinal tight junctions are selectively-permeable, and intestinal permeability can be increased physiologically in response to luminal nutrients or pathologically by mucosal immune cells and cytokines, the enteric nervous system, and pathogens. Compromised intestinal barrier function is associated with an array of clinical conditions, both intestinal and systemic. While most available data are correlative, some studies support a model where cycles of increased intestinal permeability, intestinal immune activation, and subsequent immune-mediated barrier loss contribute to disease progression. This model is applicable to intestinal and systemic diseases. However, it has not been proven and both mechanistic and therapeutic studies are ongoing. Nevertheless, the correlation between increased intestinal permeability and disease has caught the attention of the public, leading to a rise in popularity of the diagnosis of "leaky gut syndrome," which encompasses a range of systemic disorders. Proponents claim that barrier restoration will cure underlying disease, but this has not been demonstrated in clinical trials. Moreover, human and mouse studies show that intestinal barrier loss alone is insufficient to initiate disease. It is therefore uncertain if increased permeability in these patients is a cause or effect of the underlying disorder. Although drug targets that may mediate barrier restoration have been proposed, none have been proven effective. As such, current treatments for barrier dysfunction should target the underlying disease.
    Clinical gastroenterology and hepatology: the official clinical practice journal of the American Gastroenterological Association 07/2013; · 5.64 Impact Factor
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    ABSTRACT: Objective. In the K/BxN mouse model of rheumatoid arthritis, T cells reactive for the self-antigen glucose-6-phosphate isomerase (GPI) escape negative selection even though GPI expression is ubiquitous. We sought to determine whether insufficient GPI presentation could account for the failure of negative selection and development of arthritis. Methods. To increase the antigen presentation of GPI, we generated transgenic mice expressing a membrane-bound form of GPI (mGPI) and crossed them to the K/BxN mice. A monoclonal antibody specific for the alpha chain of the KRN TCR was generated to follow the fate of GPI-specific T cells. Results. mGPI transgenic mice presented GPI more efficiently and showed a dramatic increase of negative selection and an inhibition of arthritis. Interestingly, thymic negative selection remained incomplete in these mice, and the escaped autoreactive T cells were anergic in the periphery, suggesting that enhanced antigen presentation also induces peripheral tolerance. Despite this apparent tolerance induction towards GPI, these mice did go on to develop a chronic wasting disease, characterized by colonic inflammation with epithelial dysplasia, as well as a dramatic reduction in Treg cells. Conclusion. These data indicate that insufficient autoantigen expression or presentation results in defects of both central and peripheral tolerance in the K/BxN mice. It supports the idea that insufficient autoantigen levels may underlie the development of autoimmunity. © 2013 American College of Rheumatology.
    Arthritis & Rheumatology 07/2013; · 7.48 Impact Factor
  • Jerrold R. Turner
    Gastroenterology 05/2013; 144(5):1147–1148. · 12.82 Impact Factor
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    ABSTRACT: BACKGROUND & AIMS:: Tight junction dysregulation and epithelial damage contribute to barrier loss in patients with inflammatory bowel disease (IBD). However, the mechanisms that regulate these processes and their relative contributions to disease pathogenesis are incompletely understood. We investigated these processes using colitis models in mice. METHODS:: We induced colitis by adoptive transfer of CD4(+)CD45RB(hi) cells or administration of dextran sulfate sodium (DSS) to mice, including those deficient in tumor necrosis factor receptor (TNFR) 1, TNFR2, or the long isoform of myosin light chain kinase (MLCK). Intestinal tissues and isolated epithelial cells were analyzed by immunoblot, immunofluorescence, ELISA, and real-time PCR assays. RESULTS:: Induction of immune-mediated colitis by CD4(+)CD45RB(hi) adoptive transfer increased intestinal permeability; epithelial expression of claudin-2, the long isoform of MLCK, and TNFR2 (but not TNFR1); and phosphorylation of the myosin II light chain (MLC). Long MLCK upregulation, MLC phosphorylation, barrier loss, and weight loss were attenuated in TNFR2(-/-), but not TNFR1(-/-), recipients of wildtype CD4(+)CD45RB(hi) cells. Similarly, long MLCK(-/-)mice had limited increases in MLC phosphorylation, claudin-2 expression, and intestinal permeability and delayed onset of cell transfer-induced colitis. However, coincident with onset of epithelial apoptosis, colitis ultimately developed. This indicates that disease progresses via apoptosis in the absence of MLCK-dependent tight junction regulation. In support of this conclusion, long MLCK(-/-)mice were not protected from epithelial apoptosis-mediated, damage-dependent DSS colitis. CONCLUSIONS:: In immune-mediated IBD models, TNFR2 signaling increases long MLCK expression, resulting in tight junction dysregulation, barrier loss and induction of colitis. At advanced stages, colitis progresses by apoptosis and mucosal damage that results in tight junction- and MLCK-independent barrier loss. Therefore, barrier loss in immune-mediated colitis occurs via two temporally and morphologically distinct mechanisms. Differential targeting of these mechanisms may lead to improved IBD therapies.
    Gastroenterology 04/2013; · 12.82 Impact Factor
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    ABSTRACT: Whether intestinal barrier disruption precedes or is the consequence of intestinal injury in necrotizing enterocolitis (NEC) remains unknown. Using a neonatal mouse NEC model, we examined the changes in intestinal permeability and specific tight-junction (TJ) proteins preceding NEC and asked whether these changes are prevented by administration of Bifidobacterium infantis, a probiotic known to decrease NEC incidence in humans. Compared with dam-fed controls, pups submitted to the NEC protocol developed i) significantly increased intestinal permeability at 12 and 24 hours (as assessed by 70-kDa fluorescein isothiocyanate-dextran transmucosal flux); ii) occludin and claudin 4 internalization at 12 hours (as assessed by immunofluorescence and low-density membrane fraction immunoblotting); iii) increased claudin 2 expression at 6 hours and decreased claudin 4 and 7 expression at 24 hours; and iv) increased claudin 2 protein at 48 hours. Similar results were seen in human NEC, with claudin 2 protein increased. In mice, administration of B. infantis micro-organisms attenuated increases in intestinal permeability, preserved claudin 4 and occludin localization at TJs, and decreased NEC incidence. Thus, an increase in intestinal permeability precedes NEC and is associated with internalization of claudin 4 and occludin. Administration of B. infantis prevents these changes and reduces NEC incidence. The beneficial effect of B. infantis is, at least in part, due to its TJ and barrier-preserving properties.
    American Journal Of Pathology 03/2013; · 4.60 Impact Factor
  • Nature 11/2012; · 38.60 Impact Factor
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    ABSTRACT: Colonic chloride secretion is regulated via the neurohormonal and immune systems. Exogenous chemicals (e.g., butyrate, propionate) can affect chloride secretion. Capsaicin, the pungent ingredient of the chili peppers, exerts various effects on gastrointestinal function. Capsaicin is known to activate the Transient Receptor Potential Vanilloid type 1 (TRPV1), expressed in the mesenteric nervous system. Recent studies have also demonstrated its presence in epithelial cells but its role remains uncertain. Because capsaicin has been reported to inhibit colonic chloride secretion, we tested whether this effect of capsaicin could occur by direct action on epithelial cells. In mouse colon and model T84 human colonic epithelial cells, we found that capsaicin inhibited forskolin-dependent short-circuit current (FSK-Isc). Using PCR and western blot, we demonstrated the presence of TRPV1 in colonic epithelial cells. In T84 cells, TRPV1 localized at the basolateral membrane and in vesicular compartments. In permeabilized monolayers, capsaicin activated apical chloride conductance, had no effect on basolateral potassium conductance, but induced NKCC1 internalization demonstrated by immunocytochemistry and basolateral surface biotinylation. AMG-9810, a potent inhibitor of TRPV1 did not prevent the inhibition of the FSK-Isc by capsaicin. Neither resiniferatoxin nor N-Oleoyldopamine, two selective agonists of TRPV1, blocked the FSK-Isc. Conversely capsaicin, resiniferatoxin and N-Oleoyldopamine raised intracellular calcium ([Ca(2+)](i)) in T84 cells and AMG-9810 blocked the rise in [Ca(2+)](i) induced by capsaicin and resiniferatoxin suggesting the presence of a functional TRPV1 channel. We conclude that capsaicin inhibits chloride secretion in part by causing NKCC1 internalization, but by a mechanism that appears to be independent of TRPV1.
    AJP Gastrointestinal and Liver Physiology 11/2012; · 3.65 Impact Factor
  • Jerrold R Turner
    Gastroenterology 07/2012; 143(3):511-5.e1. · 12.82 Impact Factor
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    ABSTRACT: Laboratory evidence suggests that intestinal permeability is elevated following either binge ethanol exposure or burn injury alone, and this barrier dysfunction is further perturbed when these insults are combined. We and others have previously reported a rise in both systemic and local proinflammatory cytokine production in mice after the combined insult. Knowing that long myosin light-chain kinase (MLCK) is important for epithelial barrier maintenance and can be activated by proinflammatory cytokines, we examined whether inhibition of MLCK alleviated detrimental intestinal responses seen after ethanol exposure and burn injury. To accomplish this, mice were given vehicle or a single binge ethanol exposure followed by a sham or dorsal scald burn injury. Following injury, one group of mice received membrane permeant inhibitor of MLCK (PIK). At 6 and 24 h postinjury, bacterial translocation and intestinal levels of proinflammatory cytokines were measured, and changes in tight junction protein localization and total intestinal morphology were analyzed. Elevated morphological damage, ileal IL-1β and IL-6 levels, and bacterial translocation were seen in mice exposed to ethanol and burn injury relative to either insult alone. This increase was not seen in mice receiving PIK after injury. Ethanol-exposed and burn-injured mice had reduced zonula occludens protein-1 and occludin localization to the tight junction relative to sham-injured mice. However, the observed changes in junctional complexes were not seen in our PIK-treated mice following the combined insult. These data suggest that MLCK activity may promote morphological and inflammatory responses in the ileum following ethanol exposure and burn injury.
    AJP Gastrointestinal and Liver Physiology 07/2012; 303(6):G705-12. · 3.65 Impact Factor
  • Kevin E Cunningham, Jerrold R Turner
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    ABSTRACT: Dynamic regulation of paracellular permeability is essential for physiological epithelial function, while dysregulated permeability is common in disease. The recent elucidation of the molecular composition of the epithelial tight junction complex has been accompanied by characterization of diverse intracellular mediators of paracellular permeabiltiy. Myosin light chain kinase (MLCK), which induces contraction of the perijunctional actomyosin ring through myosin II regulatory light chain phosphorylation, has emerged as a key regulator of tight junction permeability. Examination of the regulation and role of MLCK in tight junction dysfunction has helped to define pathological processes and characterize the role of barrier loss in disease pathogenesis, and may provide future therapeutic targets to treat intestinal disease.
    Annals of the New York Academy of Sciences 07/2012; 1258:34-42. · 4.38 Impact Factor

Publication Stats

5k Citations
1,612.51 Total Impact Points

Institutions

  • 2013
    • The University of Chicago Medical Center
      • Department of Medicine
      Chicago, Illinois, United States
  • 2005–2013
    • University of Illinois at Chicago
      • • Department of Pathology (Chicago)
      • • Department of Medicine (Chicago)
      Chicago, Illinois, United States
  • 2002–2013
    • University of Chicago
      • • Department of Pathology
      • • Department of Medicine
      Chicago, Illinois, United States
  • 2012
    • Loyola University Medical Center
      • Burn and Shock Trauma Institute
      Maywood, Illinois, United States
  • 2007–2012
    • Medical College of Wisconsin
      • Department of Microbiology and Molecular Genetics
      Milwaukee, WI, United States
  • 2010
    • Johns Hopkins Medicine
      Baltimore, Maryland, United States
  • 2009
    • University of Tuebingen
      Tübingen, Baden-Württemberg, Germany
  • 2008
    • National Institute on Alcohol Abuse and Alcoholism
      Maryland, United States
  • 2005–2008
    • The University of Calgary
      • Department of Biological Sciences
      Calgary, Alberta, Canada
  • 2006
    • Third Military Medical University
      • Institute of Burn Research
      Chongqing, Chongqing Shi, China
  • 2002–2004
    • Wayne State University
      • Department of Pathology
      Detroit, MI, United States