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Article: Smad3 as a mediator of the fibrotic response.

Flanders, Kathleen C

International journal of experimental pathology

2004 Volume 85, Issue 2, Page(s) 47–64

Abstract: Transforming growth factor-beta (TGF-beta) plays a central role in fibrosis, contributing to the influx and activation of inflammatory cells, the epithelial to mesenchymal transdifferentiation (EMT) of cells and the influx of fibroblasts and their ... ...

Abstract	Transforming growth factor-beta (TGF-beta) plays a central role in fibrosis, contributing to the influx and activation of inflammatory cells, the epithelial to mesenchymal transdifferentiation (EMT) of cells and the influx of fibroblasts and their subsequent elaboration of extracellular matrix. TGF-beta signals through transmembrane receptor serine/threonine kinases to activate novel signalling intermediates called Smad proteins, which modulate the transcription of target genes. The use of mice with a targeted deletion of Smad3, one of the two homologous proteins which signals from TGF-beta/activin, shows that most of the pro-fibrotic activities of TGF-beta are mediated by Smad3. Smad3 null inflammatory cells and fibroblasts do not respond to the chemotactic effects of TGF-beta and do not autoinduce TGF-beta. The loss of Smad3 also interferes with TGF-beta-mediated induction of EMT and genes for collagens, plasminogen activator inhibitor-1 and the tissue inhibitor of metalloprotease-1. Smad3 null mice are resistant to radiation-induced cutaneous fibrosis, bleomycin-induced pulmonary fibrosis, carbon tetrachloride-induced hepatic fibrosis as well as glomerular fibrosis induced by induction of type 1 diabetes with streptozotocin. In fibrotic conditions that are induced by EMT, such as proliferative vitreoretinopathy, ocular capsule injury and glomerulosclerosis resulting from unilateral ureteral obstruction, Smad3 null mice also show an abrogated fibrotic response. Animal models of scleroderma, cystic fibrosis and cirrhosis implicate involvement of Smad3 in the observed fibrosis. Additionally, inhibition of Smad3 by overexpression of the inhibitory Smad7 protein or by treatment with the small molecule, halofuginone, dramatically reduces responses in animal models of kidney, lung, liver and radiation-induced fibrosis. Small moleucule inhibitors of Smad3 may have tremendous clinical potential in the treatment of pathological fibrotic diseases.
MeSH term(s)	Animals ; Cholecalciferol/therapeutic use ; Cytokines/immunology ; DNA-Binding Proteins/antagonists & inhibitors ; DNA-Binding Proteins/metabolism ; Extracellular Matrix/metabolism ; Extracellular Matrix/pathology ; Fibrosis/drug therapy ; Fibrosis/immunology ; Gene Expression Regulation ; Humans ; Signal Transduction/drug effects ; Signal Transduction/physiology ; Smad2 Protein ; Smad3 Protein ; Smad7 Protein ; Trans-Activators/antagonists & inhibitors ; Trans-Activators/metabolism ; Transforming Growth Factor beta/metabolism ; Wound Healing/physiology
Chemical Substances	Cytokines ; DNA-Binding Proteins ; SMAD2 protein, human ; SMAD3 protein, human ; SMAD7 protein, human ; Smad2 Protein ; Smad3 Protein ; Smad7 Protein ; Trans-Activators ; Transforming Growth Factor beta ; Cholecalciferol (1C6V77QF41)
Language	English
Publishing date	2004-05-06
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1016006-1
ISSN	1365-2613 ; 0959-9673 ; 0958-4625 ; 0007-1021
ISSN (online)	1365-2613
ISSN	0959-9673 ; 0958-4625 ; 0007-1021
DOI	10.1111/j.0959-9673.2004.00377.x
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Article ; Online: Transforming growth factor-β stimulates Smad1/5 signaling in pulmonary artery smooth muscle cells and fibroblasts of the newborn mouse through ALK1.

Zhang, Huili / Du, Lili / Zhong, Ying / Flanders, Kathleen C / Roberts, Jesse D

American journal of physiology. Lung cellular and molecular physiology

2017 Volume 313, Issue 3, Page(s) L615–L627

Abstract: The intracellular signaling mechanisms through which TGF-β regulates pulmonary development are incompletely understood. Canonical TGF-β signaling involves Smad2/3 phosphorylation, Smad2/3·Smad4 complex formation and nuclear localization, and gene ... ...

Abstract	The intracellular signaling mechanisms through which TGF-β regulates pulmonary development are incompletely understood. Canonical TGF-β signaling involves Smad2/3 phosphorylation, Smad2/3·Smad4 complex formation and nuclear localization, and gene regulation. Here, we show that physiologically relevant TGF-β1 levels also stimulate Smad1/5 phosphorylation, which is typically a mediator of bone morphogenetic protein (BMP) signaling, in mouse pup pulmonary artery smooth muscle cells (mPASMC) and lung fibroblasts and other interstitial lung cell lines. This cross-talk mechanism likely has in vivo relevance because mixed Smad1/5/8·Smad2/3 complexes, which are indicative of TGF-β-stimulated Smad1/5 activation, were detected in the developing mouse lung using a proximity ligation assay. Although mixed Smad complexes have been shown not to transduce nuclear signaling, we determined that TGF-β stimulates nuclear localization of phosphorylated Smad1/5 and induces the expression of prototypical BMP-regulated genes in the mPASMC. Small-molecule kinase inhibitor studies suggested that TGF-β-regulated Smad1/5 phosphorylation in these cells is mediated by TGF-β-type I receptors, not BMP-type I receptors, but possibly the accessory activin-like kinase (ALK1) receptor. Although work by others suggested that ALK1 is expressed exclusively in endothelial cells in the vasculature, we detected ALK1 mRNA and protein expression in mPASMC in vitro and in mouse pup lungs. Moreover, using an antimurine ALK1 antibody and mPASMC, we determined that ALK1 regulates Smad1/5 phosphorylation by TGF-β. Together, these studies characterize an accessory TGF-β-stimulated BMP R-Smad signaling mechanism in interstitial cells of the developing lung. They also indicate the importance of considering alternate Smad pathways in studies directed at determining how TGF-β regulates newborn lung development.
MeSH term(s)	Activin Receptors, Type I/metabolism ; Activin Receptors, Type II ; Animals ; Animals, Newborn ; Benzodioxoles/pharmacology ; Bone Morphogenetic Protein Receptors/metabolism ; Cell Line ; Cell Nucleus/drug effects ; Cell Nucleus/metabolism ; Fibroblasts/metabolism ; Humans ; Imidazoles/pharmacology ; Lung/growth & development ; Lung/metabolism ; Mice ; Myocytes, Smooth Muscle/drug effects ; Myocytes, Smooth Muscle/metabolism ; Phosphorylation/drug effects ; Protein-Serine-Threonine Kinases/metabolism ; Pulmonary Artery/cytology ; Pyridines/pharmacology ; Rats ; Receptor, Transforming Growth Factor-beta Type I ; Receptors, Transforming Growth Factor beta/metabolism ; Signal Transduction/drug effects ; Smad1 Protein/metabolism ; Smad5 Protein/metabolism ; Transforming Growth Factor beta/pharmacology
Chemical Substances	2-(5-benzo(1,3)dioxol-5-yl-2-tert-butyl-3H-imidazol-4-yl)-6-methylpyridine hydrochloride ; Benzodioxoles ; Imidazoles ; Pyridines ; Receptors, Transforming Growth Factor beta ; Smad1 Protein ; Smad5 Protein ; Transforming Growth Factor beta ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; Activin Receptors, Type I (EC 2.7.11.30) ; Activin Receptors, Type II (EC 2.7.11.30) ; Acvr1 protein, mouse (EC 2.7.11.30) ; Acvrl1 protein, mouse (EC 2.7.11.30) ; Bone Morphogenetic Protein Receptors (EC 2.7.11.30) ; Receptor, Transforming Growth Factor-beta Type I (EC 2.7.11.30) ; Tgfbr1 protein, rat (EC 2.7.11.30)
Language	English
Publishing date	2017-06-22
Publishing country	United States
Document type	Journal Article
ZDB-ID	1013184-x
ISSN	1522-1504 ; 1040-0605
ISSN (online)	1522-1504
ISSN	1040-0605
DOI	10.1152/ajplung.00079.2017
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Article ; Online: Transforming growth factor-(beta)s and mammary gland involution; functional roles and implications for cancer progression.

Flanders, Kathleen C / Wakefield, Lalage M

Journal of mammary gland biology and neoplasia

2009 Volume 14, Issue 2, Page(s) 131–144

Abstract: During rodent mammary gland involution there is a dramatic increase in the expression of the transforming growth factor-beta isoform, TGF-beta3. The TGF-betas are multifunctional cytokines which play important roles in wound healing and in carcinogenesis. ...

Abstract	During rodent mammary gland involution there is a dramatic increase in the expression of the transforming growth factor-beta isoform, TGF-beta3. The TGF-betas are multifunctional cytokines which play important roles in wound healing and in carcinogenesis. The responses that are activated in the remodeling of the gland during involution have many similarities with the wound healing process and have been postulated to generate a mammary stroma that provides a microenvironment favoring tumor progression. In this review we will discuss the putative role of TGF-beta during involution, as well as its effects on the mammary microenvironment and possible implications for pregnancy-associated tumorigenesis.
MeSH term(s)	Animals ; Apoptosis/physiology ; Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; Cicatrix/physiopathology ; Disease Progression ; Female ; Gene Expression Profiling ; Humans ; Inflammation/physiopathology ; Lactation/physiology ; Mammary Glands, Animal/physiology ; Mice ; Parity ; Pregnancy ; Pregnancy Complications, Neoplastic/physiopathology ; Prognosis ; Protein Isoforms/physiology ; RNA, Messenger/biosynthesis ; RNA, Neoplasm/biosynthesis ; Transforming Growth Factor beta/genetics ; Transforming Growth Factor beta/physiology ; Transforming Growth Factor beta3/physiology ; Treatment Outcome ; Wound Healing/physiology
Chemical Substances	Protein Isoforms ; RNA, Messenger ; RNA, Neoplasm ; Transforming Growth Factor beta ; Transforming Growth Factor beta3
Language	English
Publishing date	2009-04-25
Publishing country	United States
Document type	Journal Article
ZDB-ID	1327345-0
ISSN	1573-7039 ; 1083-3021
ISSN (online)	1573-7039
ISSN	1083-3021
DOI	10.1007/s10911-009-9122-z
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Article: Medical applications of transforming growth factor-beta.

Flanders, Kathleen C / Burmester, James K

Clinical medicine & research

2005 Volume 1, Issue 1, Page(s) 13–20

Abstract: Transforming growth factor-beta (TGF-beta) proteins and their antagonists have entered clinical trials. These multi-functional regulators of cell growth and differentiation induce extracellular matrix proteins and suppress the immune system making TGF- ... ...

Abstract	Transforming growth factor-beta (TGF-beta) proteins and their antagonists have entered clinical trials. These multi-functional regulators of cell growth and differentiation induce extracellular matrix proteins and suppress the immune system making TGF-betas useful in treatment of wounds with impaired healing, mucositis, fractures, ischemia-reperfusion injuries, and autoimmune disease. In diseases such as keloids, glomerulonephritis and pulmonary fibrosis, excessive expression of TGF-beta has been implicated as being responsible for accumulation of detrimental scar tissue. In these conditions, agents that block TGF-beta have prevented or reversed disease. Similarly, in carcinogenesis, blocking TGF-beta activity may be valuable in stimulating an immune response towards metastasis. As these blocking agents receive approval, we will likely have new therapies for previously recalcitrant diseases.
MeSH term(s)	Animals ; Autoimmune Diseases/drug therapy ; Humans ; Reperfusion Injury/drug therapy ; Transforming Growth Factor beta/chemistry ; Transforming Growth Factor beta/therapeutic use ; Wounds and Injuries/drug therapy
Chemical Substances	Transforming Growth Factor beta
Language	English
Publishing date	2005-05-25
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2303793-3
ISSN	1539-4182
ISSN	1539-4182
DOI	10.3121/cmr.1.1.13
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Article ; Online: Quantitation of TGF-β proteins in mouse tissues shows reciprocal changes in TGF-β1 and TGF-β3 in normal vs neoplastic mammary epithelium.

Flanders, Kathleen C / Yang, Yu-An / Herrmann, Michelle / Chen, JinQiu / Mendoza, Nerissa / Mirza, Amer M / Wakefield, Lalage M

Oncotarget

2016 Volume 7, Issue 25, Page(s) 38164–38179

Abstract: Transforming growth factor-βs (TGF-βs) regulate tissue homeostasis, and their expression is perturbed in many diseases. The three isoforms (TGF-β1, -β2, and -β3) have similar bioactivities in vitro but show distinct activities in vivo. Little ... ...

Abstract	Transforming growth factor-βs (TGF-βs) regulate tissue homeostasis, and their expression is perturbed in many diseases. The three isoforms (TGF-β1, -β2, and -β3) have similar bioactivities in vitro but show distinct activities in vivo. Little quantitative information exists for expression of TGF-β isoform proteins in physiology or disease. We developed an optimized method to quantitate protein levels of the three isoforms, using a Luminex® xMAP®-based multianalyte assay following acid-ethanol extraction of tissues. Analysis of multiple tissues and plasma from four strains of adult mice showed that TGF-β1 is the predominant isoform with TGF-β2 being ~10-fold lower. There were no sex-specific differences in isoform expression, but some tissues showed inter-strain variation, particularly for TGF-β2. The only adult tissue expressing appreciable TGF-β3 was the mammary gland, where its levels were comparable to TGF-β1. In situ hybridization showed the luminal epithelium as the major source of all TGF-β isoforms in the normal mammary gland. TGF-β1 protein was 3-8-fold higher in three murine mammary tumor models than in normal mammary gland, while TGF-β3 protein was 2-3-fold lower in tumors than normal tissue, suggesting reciprocal regulation of these isoforms in mammary tumorigenesis.
MeSH term(s)	Animals ; Female ; Humans ; Mammary Neoplasms, Experimental/immunology ; Mammary Neoplasms, Experimental/pathology ; Mice ; Mice, Inbred BALB C ; Protein Isoforms ; Transforming Growth Factor beta/metabolism ; Transforming Growth Factor beta1/metabolism ; Transforming Growth Factor beta3/metabolism
Chemical Substances	Protein Isoforms ; Transforming Growth Factor beta ; Transforming Growth Factor beta1 ; Transforming Growth Factor beta3
Language	English
Publishing date	2016-05-19
Publishing country	United States
Document type	Journal Article
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.9416
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Article: Transforming Growth Factor-βs and Mammary Gland Involution; Functional Roles and Implications for Cancer Progression

Flanders, Kathleen C / Wakefield, Lalage M

Journal of mammary gland biology and neoplasia. 2009 June, v. 14, no. 2

2009

Abstract: During rodent mammary gland involution there is a dramatic increase in the expression of the transforming growth factor-β isoform, TGF-β3. The TGF-βs are multifunctional cytokines which play important roles in wound healing and in carcinogenesis. The ... ...

Abstract	During rodent mammary gland involution there is a dramatic increase in the expression of the transforming growth factor-β isoform, TGF-β3. The TGF-βs are multifunctional cytokines which play important roles in wound healing and in carcinogenesis. The responses that are activated in the remodeling of the gland during involution have many similarities with the wound healing process and have been postulated to generate a mammary stroma that provides a microenvironment favoring tumor progression. In this review we will discuss the putative role of TGF-β during involution, as well as its effects on the mammary microenvironment and possible implications for pregnancy-associated tumorigenesis.
Language	English
Dates of publication	2009-06
Size	p. 131-144.
Publisher	Springer US
Publishing place	Boston
Document type	Article
ZDB-ID	1327345-0
ISSN	1083-3021
ISSN	1083-3021
DOI	10.1007/s10911-009-9122-z
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Article ; Online: Inhibition of development of laser-induced choroidal neovascularization with suppression of infiltration of macrophages in Smad3-null mice.

Iwanishi, Hiroki / Fujita, Norihito / Tomoyose, Katsuo / Okada, Yuka / Yamanaka, Osamu / Flanders, Kathleen C / Saika, Shizuya

Laboratory investigation; a journal of technical methods and pathology

2016 Volume 96, Issue 6, Page(s) 641–651

Abstract: We evaluated the effects of the loss of Smad3 on the development of experimental argon laser-induced choroidal neovascularization (CNV) in mice. An in vitro angiogenesis model was also used to examine the role of transforming growth factor-β1 (TGFβ1)/ ... ...

Abstract	We evaluated the effects of the loss of Smad3 on the development of experimental argon laser-induced choroidal neovascularization (CNV) in mice. An in vitro angiogenesis model was also used to examine the role of transforming growth factor-β1 (TGFβ1)/Smad3 signaling in vessel-like tube formation by human umbilical vein endothelial cells (HUVECs). CNV was induced in eyes of 8-12-week-old B6.129-background Smad3-deficient (KO) mice (n=47) and wild-type (WT) mice (n=47) by argon laser irradiation. Results showed that the size of the CNV induced was significantly smaller in KO mice as compared with WT mice at day 14 as revealed by high-resolution angiography with fluorescein isothiocyanate-dextran. Immunohistochemistry and real-time reverse transcription-polymerase chain reaction of RNA extracted from laser-irradiated choroidal tissues were conducted on specimens at specific timepoints. Invasion of macrophages (F4/80+), but not neutrophils (myeloperoxidase+), and appearance of myofibroblasts (α-smooth muscle actin+) were suppressed in laser-irradiated KO tissues. mRNA expression of inflammation-related factors, that is, vascular endothelial growth factor (VEGF), macrophage-chemoattractant protein-1 (MCP-1), interleukin-6 (IL-6) and TGFβ1 in choroidal tissues was suppressed by the loss of Smad3. We then examined the effects of adding a Smad3 inhibitor, SIS3, or an ALK5 inhibitor, SB431542, on tube formation promoted by TGFβ1 or VEGF in HUVECs cocultured with fibroblast feeder. Further addition of SIS3 or SB431542 augmented vessel-like tube formation by HUVECs in the presence of TGFβ1 or VEGF. In conclusion, lack of Smad3 attenuated the growth of laser-induced CNV with suppression of inflammation by macrophages in mice. Because blocking TGFβ1/Smad3 signal stimulated the activity of angiogenesis of HUVECs in vitro, the reduction of CNV in vivo in KO mice is attributed to a decrease in growth factor levels in the tissue by the loss of Smad3.
MeSH term(s)	Animals ; Choroidal Neovascularization/etiology ; Choroidal Neovascularization/pathology ; Choroidal Neovascularization/prevention & control ; Disease Models, Animal ; Human Umbilical Vein Endothelial Cells ; Humans ; Inflammation Mediators/metabolism ; Isoquinolines/pharmacology ; Lasers, Gas/adverse effects ; Macrophages/pathology ; Male ; Mice ; Mice, 129 Strain ; Mice, Inbred C57BL ; Mice, Knockout ; Pyridines/pharmacology ; Pyrroles/pharmacology ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Smad3 Protein/antagonists & inhibitors ; Smad3 Protein/deficiency ; Smad3 Protein/genetics ; Transforming Growth Factor beta1
Chemical Substances	6,7-dimethyl-2-(2E)-3-(1-methyl-2-phenyl-1H-pyrrolo(2,3-b)pyridin-3-yl-prop-2-enoyl)-1,2,3,4-tetrahydroisoquinoline hydrochloride ; Inflammation Mediators ; Isoquinolines ; Pyridines ; Pyrroles ; RNA, Messenger ; SMAD3 protein, human ; Smad3 Protein ; Smad3 protein, mouse ; TGFB1 protein, human ; Transforming Growth Factor beta1
Language	English
Publishing date	2016-03-07
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80178-1
ISSN	1530-0307 ; 0023-6837
ISSN (online)	1530-0307
ISSN	0023-6837
DOI	10.1038/labinvest.2016.30
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Article ; Online: Impaired healing of cornea incision injury in a TRPV1-deficient mouse.

Nidegawa-Saitoh, Yuka / Sumioka, Takayoshi / Okada, Yuka / Reinach, Peter S / Flanders, Kathleen C / Liu, Chia-Yang / Yamanaka, Osamu / Kao, Winston Whei-Yang / Saika, Shizuya

Cell and tissue research

2018 Volume 374, Issue 2, Page(s) 329–338

Abstract: The present study attempts to elucidate the role of TRPV1 cation channel receptor on primary repair in an incision-wounded mouse cornea in vivo. Previous study revealed that blocking TRPV1 suppressed myofibroblast formation and expression of transforming ...

Abstract	The present study attempts to elucidate the role of TRPV1 cation channel receptor on primary repair in an incision-wounded mouse cornea in vivo. Previous study revealed that blocking TRPV1 suppressed myofibroblast formation and expression of transforming growth factor β1 (TGFβ1) in cultured keratocytes or ocular fibroblasts. Male C57BL/6 (wild-type; WT) mice and male C57BL/6 Trpv1-null (KO) mice incurred a full-thickness incision injury (1.8 mm in length, limbus to limbus) in the central cornea of one eye with a surgical blade under general and topical anesthesia. The injury was not sutured. On days 0, 5, and 10, the eyes were enucleated, processed for histology, immunohistochemistry, and real-time RT-PCR gene expression analysis to evaluate the effects of the loss of TRPV1 on primary healing. Electron microscopy observation was also performed to know the effect of the loss of TRPV1 on ultrastructure of keratocytes. The results showed that the loss of Trpv1 gene delayed closure of corneal stromal incision with hindered myofibroblast transdifferentiation along with declines in the expression of collagen Ia1 and TGFβ1. Inflammatory cell infiltration was not affected by the loss of TRPV1. Ultrastructurally endoplasmic reticulum of TRPV1-null keratocytes was more extensively dilated as compared with WT keratocytes, suggesting an impairment of protein secretion by TRPV1-gene knockout. These results indicate that injury-related TRPV1 signal is involved in healing of stromal incision injury in a mouse cornea by selectively stimulating TGFβ-induced granulation tissue formation.
MeSH term(s)	Animals ; Cornea/pathology ; Cornea/ultrastructure ; Corneal Injuries/metabolism ; Corneal Injuries/pathology ; Inflammation/pathology ; Male ; Mice, Inbred C57BL ; Mice, Knockout ; Myofibroblasts/pathology ; TRPV Cation Channels/deficiency ; TRPV Cation Channels/metabolism ; Transforming Growth Factor beta/metabolism ; Wound Healing
Chemical Substances	TRPV Cation Channels ; TRPV1 protein, mouse ; Transforming Growth Factor beta
Language	English
Publishing date	2018-07-04
Publishing country	Germany
Document type	Journal Article
ZDB-ID	125067-x
ISSN	1432-0878 ; 0302-766X
ISSN (online)	1432-0878
ISSN	0302-766X
DOI	10.1007/s00441-018-2878-y
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Article: Impaired healing of cornea incision injury in a TRPV1-deficient mouse

Nidegawa-Saitoh, Yuka / Sumioka, Takayoshi / Okada, Yuka / Reinach, Peter S / Flanders, Kathleen C / Liu, Chia-Yang / Yamanaka, Osamu / Kao, Winston Whei-Yang / Saika, Shizuya

Cell and tissue research. 2018 Nov., v. 374, no. 2

2018

Abstract	The present study attempts to elucidate the role of TRPV1 cation channel receptor on primary repair in an incision-wounded mouse cornea in vivo. Previous study revealed that blocking TRPV1 suppressed myofibroblast formation and expression of transforming growth factor β1 (TGFβ1) in cultured keratocytes or ocular fibroblasts. Male C57BL/6 (wild-type; WT) mice and male C57BL/6 Trpv1-null (KO) mice incurred a full-thickness incision injury (1.8 mm in length, limbus to limbus) in the central cornea of one eye with a surgical blade under general and topical anesthesia. The injury was not sutured. On days 0, 5, and 10, the eyes were enucleated, processed for histology, immunohistochemistry, and real-time RT-PCR gene expression analysis to evaluate the effects of the loss of TRPV1 on primary healing. Electron microscopy observation was also performed to know the effect of the loss of TRPV1 on ultrastructure of keratocytes. The results showed that the loss of Trpv1 gene delayed closure of corneal stromal incision with hindered myofibroblast transdifferentiation along with declines in the expression of collagen Ia1 and TGFβ1. Inflammatory cell infiltration was not affected by the loss of TRPV1. Ultrastructurally endoplasmic reticulum of TRPV1-null keratocytes was more extensively dilated as compared with WT keratocytes, suggesting an impairment of protein secretion by TRPV1-gene knockout. These results indicate that injury-related TRPV1 signal is involved in healing of stromal incision injury in a mouse cornea by selectively stimulating TGFβ-induced granulation tissue formation.
Keywords	anesthesia ; collagen ; cornea ; electron microscopy ; endoplasmic reticulum ; fibroblasts ; gene expression ; genes ; granulation tissue ; immunohistochemistry ; ion channels ; males ; mice ; quantitative polymerase chain reaction ; reverse transcriptase polymerase chain reaction ; transforming growth factor beta 1 ; ultrastructure
Language	English
Dates of publication	2018-11
Size	p. 329-338.
Publishing place	Springer Berlin Heidelberg
Document type	Article
ZDB-ID	125067-x
ISSN	1432-0878 ; 0302-766X
ISSN (online)	1432-0878
ISSN	0302-766X
DOI	10.1007/s00441-018-2878-y
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Clinical Practice Guidelines for the Perioperative Nutrition, Metabolic, and Nonsurgical Support of Patients Undergoing Bariatric Procedures - 2019 Update: Cosponsored by American Association of Clinical Endocrinologists/American College of Endocrinology, The Obesity Society, American Society for Metabolic and Bariatric Surgery, Obesity Medicine Association, and American Society of Anesthesiologists.

Obesity (Silver Spring, Md.)

2020 Volume 28, Issue 4, Page(s) O1–O58

Abstract: ... 17%) Grade B, 72 (29%) Grade C, and 101 (41%) Grade D recommendations. There are 858 citations ...

Abstract	Objective: The development of these updated clinical practice guidelines (CPGs) was commissioned by the American Association of Clinical Endocrinologists (AACE), The Obesity Society (TOS), American Society for Metabolic and Bariatric Surgery (ASMBS), Obesity Medicine Association (OMA), and American Society of Anesthesiologists (ASA) Boards of Directors in adherence with the AACE 2017 protocol for standardized production of CPGs, algorithms, and checklists. Methods: Each recommendation was evaluated and updated based on new evidence from 2013 to the present and subjective factors provided by experts. Results: New or updated topics in this CPG include: contextualization in an adiposity-based chronic disease complications-centric model, nuance-based and algorithm/checklist-assisted clinical decision-making about procedure selection, novel bariatric procedures, enhanced recovery after bariatric surgery protocols, and logistical concerns (including cost factors) in the current health care arena. There are 85 numbered recommendations that have updated supporting evidence, of which 61 are revised and 12 are new. Noting that there can be multiple recommendation statements within a single numbered recommendation, there are 31 (13%) Grade A, 42 (17%) Grade B, 72 (29%) Grade C, and 101 (41%) Grade D recommendations. There are 858 citations, of which 81 (9.4%) are evidence level (EL) 1 (highest), 562 (65.5%) are EL 2, 72 (8.4%) are EL 3, and 143 (16.7%) are EL 4 (lowest). Conclusions: Bariatric procedures remain a safe and effective intervention for higher-risk patients with obesity. Clinical decision-making should be evidence based within the context of a chronic disease. A team approach to perioperative care is mandatory, with special attention to nutritional and metabolic issues.
MeSH term(s)	Bariatric Surgery/methods ; Bariatric Surgery/standards ; Bariatrics/methods ; Bariatrics/standards ; Female ; Humans ; Male ; Obesity/therapy
Language	English
Publishing date	2020-03-21
Publishing country	United States
Document type	Journal Article ; Practice Guideline
ZDB-ID	2230457-5
ISSN	1930-739X ; 1071-7323 ; 1930-7381
ISSN (online)	1930-739X
ISSN	1071-7323 ; 1930-7381
DOI	10.1002/oby.22719
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