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Vicente, A., Sloniecka, M., Liu, J.-X., Byström, B. & Domellöf, F. P. (2022). Aniridia-related keratopathy relevant cell signaling pathways in human fetal corneas. Histochemistry and Cell Biology, 158(2), 169-180
Åpne denne publikasjonen i ny fane eller vindu >>Aniridia-related keratopathy relevant cell signaling pathways in human fetal corneas
Vise andre…
2022 (engelsk)Inngår i: Histochemistry and Cell Biology, ISSN 0948-6143, E-ISSN 1432-119X, Vol. 158, nr 2, s. 169-180Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

We aimed to study aniridia-related keratopathy (ARK) relevant cell signaling pathways [Notch1, Wnt/β-catenin, Sonic hedgehog (SHH) and mTOR] in normal human fetal corneas compared with normal human adult corneas and ARK corneas. We found that fetal corneas at 20 weeks of gestation (wg) and normal adult corneas showed similar staining patterns for Notch1; however 10–11 wg fetal corneas showed increased presence of Notch1. Numb and Dlk1 had an enhanced presence in the fetal corneas compared with the adult corneas. Fetal corneas showed stronger immunolabeling with antibodies against β-catenin, Wnt5a, Wnt7a, Gli1, Hes1, p-rpS6, and mTOR when compared with the adult corneas. Gene expression of Notch1, Wnt5A, Wnt7A, β-catenin, Hes1, mTOR, and rps6 was higher in the 9–12 wg fetal corneas compared with adult corneas. The cell signaling pathway differences found between human fetal and adult corneas were similar to those previously found in ARK corneas with the exception of Notch1. Analogous profiles of cell signaling pathway activation between human fetal corneas and ARK corneas suggests that there is a less differentiated host milieu in ARK.

sted, utgiver, år, opplag, sider
Springer, 2022
Emneord
Aniridia, Fetal cornea, Adult cornea, Sonic hedgehog, Notch, mTOR, Wnt
HSV kategori
Identifikatorer
urn:nbn:se:umu:diva-164256 (URN)10.1007/s00418-022-02099-9 (DOI)000799082100002 ()35551459 (PubMedID)2-s2.0-85129792626 (Scopus ID)
Forskningsfinansiär
Region VästerbottenUmeå UniversityStiftelsen Kronprinsessan Margaretas arbetsnämnd för synskadadeÅke Wiberg Foundation
Merknad

Originally included in thesis in manuscript form.

Tilgjengelig fra: 2019-10-18 Laget: 2019-10-18 Sist oppdatert: 2023-09-05bibliografisk kontrollert
Sloniecka, M. & Danielson, P. (2020). Acetylcholine decreases formation of myofibroblasts and excessive extracellular matrix production in an in vitro human corneal fibrosis model. Journal of Cellular and Molecular Medicine (Print), 24(8), 4850-4862
Åpne denne publikasjonen i ny fane eller vindu >>Acetylcholine decreases formation of myofibroblasts and excessive extracellular matrix production in an in vitro human corneal fibrosis model
2020 (engelsk)Inngår i: Journal of Cellular and Molecular Medicine (Print), ISSN 1582-1838, E-ISSN 1582-4934, Vol. 24, nr 8, s. 4850-4862Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Acetylcholine (ACh) has been reported to play various physiological roles, including wound healing in the cornea. Here, we study the role of ACh in the transition of corneal fibroblasts into myofibroblasts, and in consequence its role in the onset of fibrosis, in an in vitro human corneal fibrosis model. Primary human keratocytes were obtained from healthy corneas. Vitamin C (VitC) and transforming growth factor-β1 (TGF-β1) were used to induce fibrosis in corneal fibroblasts. qRT-PCR and ELISA analyses showed that gene expression and production of collagen I, collagen III, collagen V, lumican, fibronectin (FN) and alpha-smooth muscle actin (α-SMA) were reduced by ACh in quiescent keratocytes. ACh treatment furthermore decreased gene expression and production of collagen I, collagen III, collagen V, lumican, FN and α-SMA during the transition of corneal fibroblasts into myofibroblasts, after induction of fibrotic process. ACh inhibited corneal fibroblasts from developing contractile activity during the process of fibrosis, as assessed with collagen gel contraction assay. Moreover, the effect of ACh was dependent on activation of muscarinic ACh receptors. These results show that ACh has an anti-fibrotic effect in an in vitro human corneal fibrosis model, as it negatively affects the transition of corneal fibroblasts into myofibroblasts. Therefore, ACh might play a role in the onset of fibrosis in the corneal stroma.

sted, utgiver, år, opplag, sider
John Wiley & Sons, 2020
Emneord
collagens, cornea, fibrotic markers, keratocytes, scarring
HSV kategori
Identifikatorer
urn:nbn:se:umu:diva-170515 (URN)10.1111/jcmm.15168 (DOI)000527848000043 ()32176460 (PubMedID)2-s2.0-85081750271 (Scopus ID)
Tilgjengelig fra: 2020-05-07 Laget: 2020-05-07 Sist oppdatert: 2023-03-24bibliografisk kontrollert
Sloniecka, M. & Danielson, P. (2019). Substance P induces fibrotic changes through activation of the RhoA/ROCK pathway in an in vitro human corneal fibrosis model. Journal of Molecular Medicine, 97(10), 1477-1489
Åpne denne publikasjonen i ny fane eller vindu >>Substance P induces fibrotic changes through activation of the RhoA/ROCK pathway in an in vitro human corneal fibrosis model
2019 (engelsk)Inngår i: Journal of Molecular Medicine, ISSN 0946-2716, E-ISSN 1432-1440, Vol. 97, nr 10, s. 1477-1489Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Fibrosis is characterized by hardening, overgrowth, and development of scars in various tissues as a result of faulty reparative processes, diseases, or chronic inflammation. During the fibrotic process in the corneal stroma of the eye, the resident cells called keratocytes differentiate into myofibroblasts, specialized contractile fibroblastic cells that produce excessive amounts of disorganized extracellular matrix (ECM) and pro-fibrotic components such as alpha-smooth muscle actin (alpha-SMA) and fibronectin. This study aimed to elucidate the role of substance P (SP), a neuropeptide that has been shown to be involved in corneal wound healing, in ECM production and fibrotic markers expression in quiescent human keratocytes, and during the onset of fibrosis in corneal fibroblasts, in an in vitro human corneal fibrosis model. We report that SP induces keratocyte contraction and upregulates gene expression of collagens I, III, and V, and fibrotic markers: alpha-SMA and fibronectin, in keratocytes. Using our in vitro human corneal fibrosis model, we show that SP enhances gene expression and secretion of collagens I, III, and V, and lumican. Moreover, SP upregulates gene expression and secretion of alpha-SMA and fibronectin, and increases contractility of corneal fibroblasts during the onset of fibrosis. Activation of the preferred SP receptor, the neurokinin-1 receptor (NK-1R), is necessary for the SP-induced pro-fibrotic changes. In addition, SP induces the pro-fibrotic changes through activation of the RhoA/ROCK pathway. Taken together, we show that SP has a pro-fibrotic effect in both quiescent human keratocytes and during the onset of fibrosis in an in vitro human corneal fibrosis model.

sted, utgiver, år, opplag, sider
Springer Berlin/Heidelberg, 2019
Emneord
Cornea, Keratocytes, Scarring, Collagens, Fibrotic markers
HSV kategori
Identifikatorer
urn:nbn:se:umu:diva-164380 (URN)10.1007/s00109-019-01827-4 (DOI)000486177200009 ()31399750 (PubMedID)2-s2.0-85070259214 (Scopus ID)
Tilgjengelig fra: 2019-11-12 Laget: 2019-11-12 Sist oppdatert: 2023-03-24bibliografisk kontrollert
Sloniecka, M. & Danielson, P. (2018). Acetylcholine decreases formation of myofibroblasts and excessive extracellular matrix components production in an in vitro human corneal fibrosis model. Paper presented at Annual Meeting of the Association-for-Research-in-Vision-and-Ophthalmology (ARVO), APR 29-MAY 03, 2018, Honolulu, HI. Investigative Ophthalmology and Visual Science, 59(9)
Åpne denne publikasjonen i ny fane eller vindu >>Acetylcholine decreases formation of myofibroblasts and excessive extracellular matrix components production in an in vitro human corneal fibrosis model
2018 (engelsk)Inngår i: Investigative Ophthalmology and Visual Science, ISSN 0146-0404, E-ISSN 1552-5783, Vol. 59, nr 9Artikkel i tidsskrift, Meeting abstract (Annet vitenskapelig) Published
Abstract [en]

Purpose : Acetylcholine (ACh) is a neurotransmitter present in corneal stroma and produced by keratocytes. It has been shown to play a role in processes important for wound healing. Based on literature and our previous studies, we hypothesize that ACh regulates expression of extracellular matrix (ECM) components that are overexpressed during fibrosis, such as collagens, proteoglycans, fibronectin and metalloproteinases, in a protective manner during corneal fibrosis, i.e. decreasing their expression.

Methods : Primary keratocytes were isolated from healthy human corneas obtained from the local cornea bank and grown in presence of 10% fetal bovine serum in order to obtain corneal fibroblasts. A corneal fibrosis in vitro model, in which fibroblasts are stimulated with transforming growth factor beta 1 (TGF-β1) and stable vitamin C, was used throughout this study. Contractile ability of myofibroblasts was tested using a cell contraction assay. Gene expression of ECM components (collagen I, collagen III, collagen V and lumican), markers of fibrosis (α-smooth muscle actin [α-SMA] and fibronectin), and metalloproteinases (MMP2, MMP9 and MMP12) were assessed by qRT-PCR. Intracellular production and secretion of pro-collagen I and lumican was determined by ELISA. α-SMA protein expression was assessed by western blot.

Results : ACh decreased the contractile ability of the newly formed myofibroblasts. ACh significantly decreased gene expression of collagen I, collagen III and collagen V in myofibroblasts. Moreover, ACh treated cells produced and secreted less pro-collagen I. Gene expression of lumican was unaffected by ACh treatment up to day 2 but significantly decreased by day 4. However, no differences in lumican protein level, both intracellular and secreted, were found. ACh downregulated expression of both α-SMA and fibronectin genes. Additionally, α-SMA protein expression was also diminished in ACh treated cells. Furthermore, ACh treatment resulted in downregulation of MMP2, MMP9 and MMP12 genes.

Conclusions : Our results are consistent with our hypothesis that ACh regulates expression of various collagens, lumican, fibronectin and metalloproteinases during corneal fibrosis in vitro, in a way that it diminishes their expression, both on RNA and protein levels. In conclusion, ACh seems to provide protection against formation of fibrosis in human cornea.

sted, utgiver, år, opplag, sider
The Association for Research in Vision and Ophthalmology, Inc., 2018
HSV kategori
Identifikatorer
urn:nbn:se:umu:diva-152274 (URN)000442912506279 ()
Konferanse
Annual Meeting of the Association-for-Research-in-Vision-and-Ophthalmology (ARVO), APR 29-MAY 03, 2018, Honolulu, HI
Forskningsfinansiär
Swedish Research Council, 521-2013-2612The Kempe Foundations, JCK-1222Swedish Society of Medicine, SLS-410021Swedish Society of Medicine, SLS-410021Västerbotten County Council, VLL-363161Västerbotten County Council, VLL-549761
Tilgjengelig fra: 2018-10-02 Laget: 2018-10-02 Sist oppdatert: 2018-10-02bibliografisk kontrollert
Sloniecka, M. & Danielson, P. (2018). Substance P Promotes Fibrosis in Human Corneal Stroma. Paper presented at 30th Annual Meeting of the Wound Healing SocietySAWC-Spring/WHS Joint Meeting, Charlotte Convention Center, Charlotte, North Carolina, USAApril 25–29, 2018. Wound Repair and Regeneration, 26(1), A22-A22, Article ID N4.05.
Åpne denne publikasjonen i ny fane eller vindu >>Substance P Promotes Fibrosis in Human Corneal Stroma
2018 (engelsk)Inngår i: Wound Repair and Regeneration, ISSN 1067-1927, E-ISSN 1524-475X, Vol. 26, nr 1, s. A22-A22, artikkel-id N4.05Artikkel i tidsskrift, Meeting abstract (Annet vitenskapelig) Published
Abstract [en]

Substance P (SP) is a neuropeptide which has been shown to be present in human corneal cells, keratocytes. Many studies suggest its role in various cellular processes important in wound healing such as proliferation or migration. We hypothesize that SP regulates expression of keratocyte markers, extracellular matrix (ECM) components and fibrotic markers that are overexpressed during fibrosis, in both primary keratocytes and myofibroblasts. Primary keratocytes, which were isolated from healthy human corneas obtained from the local cornea bank, and an in vitro corneal fibrosis model (myofibroblasts) were used throughout this study. The effect of SP on keratocyte and myofibroblast contractile abilities was assessed by cell contraction assay. Gene expression of keratocyte markers (keratocan and aldehyde dehydrogenase 3 family, member A1 [ALDH3A1]), ECM components (collagen I, collagen III, collagen V and lumican), and markers of fibrosis (a-smooth muscle actin [a-SMA] and fibronectin), was determined by qRT-PCR. Treatment of keratocytes with SP resulted in decreased expression of keratocan gene but increased ALDH3A expression. SP increased expression of fibrotic markers, a-SMA and fibronectin. Moreover, collagen I, collagen III and collagen V genes were also up-regulated by SP. Expression of lumican was unaffected by SP. Furthermore, keratocytes treated with SP showed increased contractile abilities. Similar effects of SP were observed in the corneal fibrosis model. SP decreased keratocan, but increased ALDH3A1 gene expression. a-SMA, fibronectin, collagen I, collagen III and collagen V genes were up-regulated. Expression of lumican was unaffected. Contractile abilities of myofibroblasts increased upon SP treatment. In conclusion, SP is able to regulate keratocyte marker genes and to increase expression of various ECM genes and fibrotic markers in both keratocytes and myofibroblasts. This suggests that SP might promote fibrosis in human cornea.

sted, utgiver, år, opplag, sider
Wound Healing Society, 2018
HSV kategori
Identifikatorer
urn:nbn:se:umu:diva-148839 (URN)000430308600088 ()
Konferanse
30th Annual Meeting of the Wound Healing SocietySAWC-Spring/WHS Joint Meeting, Charlotte Convention Center, Charlotte, North Carolina, USAApril 25–29, 2018
Tilgjengelig fra: 2018-06-12 Laget: 2018-06-12 Sist oppdatert: 2020-03-11bibliografisk kontrollert
El-Habta, R., Sloniecka, M., Kingham, P. J. & Backman, L. J. (2018). The adipose tissue stromal vascular fraction secretome enhances the proliferation but inhibits the differentiation of myoblasts. Stem Cell Research & Therapy, 9, Article ID 352.
Åpne denne publikasjonen i ny fane eller vindu >>The adipose tissue stromal vascular fraction secretome enhances the proliferation but inhibits the differentiation of myoblasts
2018 (engelsk)Inngår i: Stem Cell Research & Therapy, E-ISSN 1757-6512, Vol. 9, artikkel-id 352Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Background: Adipose tissue is an excellent source for isolation of stem cells for treating various clinical conditions including injuries to the neuromuscular system. Many previous studies have focused on differentiating these adipose stem cells (ASCs) towards a Schwann cell-like phenotype (dASCs), which can enhance axon regeneration and reduce muscle atrophy. However, the stromal vascular fraction (SVF), from which the ASCs are derived, also exerts broad regenerative potential and might provide a faster route to clinical translation of the cell therapies for treatment of neuromuscular disorders.

Methods: The aim of this study was to establish the effects of SVF cells on the proliferation and differentiation of myoblasts using indirect co-culture experiments. A Growth Factor PCR Array was used to compare the secretomes of SVF and dASCs, and the downstream signaling pathways were investigated.

Results: SVF cells, unlike culture-expanded dASCs, expressed and secreted hepatocyte growth factor (HGF) at concentrations sufficient to enhance the proliferation of myoblasts. Pharmacological inhibitor studies revealed that the signal is mediated via ERK1/2 phosphorylation and that the effect is significantly reduced by the addition of 100 pM Norleual, a specific HGF inhibitor. When myoblasts were differentiated into multinucleated myotubes, the SVF cells reduced the expression levels of fast-type myosin heavy chain (MyHC2) suggesting an inhibition of the differentiation process.

Conclusions: In summary, this study shows the importance of HGF as a mediator of the SVF effects on myoblasts and provides further evidence for the importance of the secretome in cell therapy and regenerative medicine applications.

sted, utgiver, år, opplag, sider
BioMed Central, 2018
Emneord
Adipose stem cells, Differentiation, HGF, Myoblasts, Myotubes, Myogenesis, Proliferation, SVF
HSV kategori
Identifikatorer
urn:nbn:se:umu:diva-155097 (URN)10.1186/s13287-018-1096-6 (DOI)000454165400001 ()30572954 (PubMedID)2-s2.0-85058900109 (Scopus ID)
Tilgjengelig fra: 2019-01-10 Laget: 2019-01-10 Sist oppdatert: 2023-03-24bibliografisk kontrollert
Sloniecka, M. U. & Danielson, P. (2017). Acetylcholine regulates expression of lumican and collagen i in keratocytes in quiescent state and after transitioning to fibroblasts and myofibroblasts. Wound Repair and Regeneration, 25(4), A32-A32
Åpne denne publikasjonen i ny fane eller vindu >>Acetylcholine regulates expression of lumican and collagen i in keratocytes in quiescent state and after transitioning to fibroblasts and myofibroblasts
2017 (engelsk)Inngår i: Wound Repair and Regeneration, ISSN 1067-1927, E-ISSN 1524-475X, Vol. 25, nr 4, s. A32-A32Artikkel i tidsskrift, Meeting abstract (Annet vitenskapelig) Published
sted, utgiver, år, opplag, sider
WILEY, 2017
HSV kategori
Identifikatorer
urn:nbn:se:umu:diva-143673 (URN)000416631700136 ()
Tilgjengelig fra: 2018-01-16 Laget: 2018-01-16 Sist oppdatert: 2018-06-09bibliografisk kontrollert
Sloniecka, M., Backman, L. J. & Danielson, P. (2016). Antiapoptotic Effect of Acetylcholine in Fas-Induced Apoptosis in Human Keratocytes. Investigative Ophthalmology and Visual Science, 57(14), 5892-5902
Åpne denne publikasjonen i ny fane eller vindu >>Antiapoptotic Effect of Acetylcholine in Fas-Induced Apoptosis in Human Keratocytes
2016 (engelsk)Inngår i: Investigative Ophthalmology and Visual Science, ISSN 0146-0404, E-ISSN 1552-5783, Vol. 57, nr 14, s. 5892-5902Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

PURPOSE. To investigate the possible antiapoptotic effect of acetylcholine (ACh) in Fas-mediated apoptosis of primary human keratocytes in vitro, and to explore the underlying mechanism. METHODS. Primary human keratocytes were isolated from healthy corneas. Fas ligand (FasL) was used to induce apoptosis in keratocytes. Cell death was assessed by ELISA. Activity of caspase-3, -7, -8, and -9 was measured with luminescent caspase activity assays. Expression of nuclear factor-kappa B (NF-kappa B) gene was assessed with RT-quantitative (q)PCR. Cytochrome c release apoptosis assay kit was used to extract mitochondria and cytosol. Cytochrome c release, cleavage of Bid, and expression of B-cell lymphoma 2 (Bcl-2) were determined by Western blot. RESULTS. Cell death ELISA revealed that ACh is able to reduce Fas-induced apoptosis in keratocytes. Analysis of the activity of effector caspases-3 and -7 showed that ACh, when added to Fas-treated cells, decreases the activation of both these enzymes. The activity of initiator caspases -8 and -9 also decreased when ACh was added to Fas-treated cells. This antiapoptotic effect of ACh was dependent on ACh concentration and activation of muscarinic ACh receptors. Analysis of the antiapoptotic mechanisms triggered by ACh showed that ACh downregulates expression of FasL-induced NF-kappa B RNA expression, upregulates expression of antiapoptotic protein Bcl-2, downregulates expression of proapoptotic protein Bad, reduces cytochrome c release, and prevents proapoptotic Bid protein cleavage. CONCLUSIONS. Acetylcholine has an antiapoptotic effect in a Fas-apoptosis model of human primary keratocytes in vitro. It is therefore possible that ACh may play a role in corneal wound healing, by modulating its initiation phase.

Emneord
Bcl-2, cytochrome c, muscarinic acetylcholine receptors, caspases, cornea
HSV kategori
Identifikatorer
urn:nbn:se:umu:diva-131665 (URN)10.1167/iovs.16-19707 (DOI)000392380000006 ()27802519 (PubMedID)2-s2.0-84994493706 (Scopus ID)
Tilgjengelig fra: 2017-02-24 Laget: 2017-02-24 Sist oppdatert: 2023-03-23bibliografisk kontrollert
Erttmann, S. F., Härtlova, A., Sloniecka, M., Raffi, F. A. M., Hosseinzadeh, A., Edgren, T., . . . Gekara, N. O. (2016). Loss of the DNA Damage Repair Kinase ATM Impairs Inflammasome-Dependent Anti-Bacterial Innate Immunity. Immunity, 45(1), 106-118
Åpne denne publikasjonen i ny fane eller vindu >>Loss of the DNA Damage Repair Kinase ATM Impairs Inflammasome-Dependent Anti-Bacterial Innate Immunity
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2016 (engelsk)Inngår i: Immunity, ISSN 1074-7613, E-ISSN 1097-4180, Vol. 45, nr 1, s. 106-118Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

The ATM kinase is a central component of the DNA damage repair machinery and redox balance. ATM dysfunction results in the multisystem disease ataxia-telangiectasia (AT). A major cause of mortality in AT is respiratory bacterial infections. Whether ATM deficiency causes innate immune defects that might contribute to bacterial infections is not known. Here we have shown that loss of ATM impairs inflammasome- dependent anti-bacterial innate immunity. Cells from AT patients or Atm(-/-) mice exhibited diminished interleukin-1 beta (IL-1 beta) production in response to bacteria. In vivo, Atm(-/-) mice were more susceptible to pulmonary S. pneumoniae infection in a manner consistent with inflammasome defects. Our data indicate that such defects were due to oxidative inhibition of inflammasome complex assembly. This study reveals an unanticipated function of reactive oxygen species (ROS) in negative regulation of inflammasomes and proposes a theory for the notable susceptibility of AT patients to pulmonary bacterial infection.

HSV kategori
Identifikatorer
urn:nbn:se:umu:diva-125590 (URN)10.1016/j.immuni.2016.06.018 (DOI)000380749000014 ()27421701 (PubMedID)2-s2.0-84990818455 (Scopus ID)
Tilgjengelig fra: 2016-09-23 Laget: 2016-09-13 Sist oppdatert: 2024-04-11bibliografisk kontrollert
Sloniecka, M., Le Roux, S., Zhou, Q. & Danielson, P. (2016). Substance P Enhances Keratocyte Migration and Neutrophil Recruitment through Interleukin-8. Molecular Pharmacology, 89(2), 215-225
Åpne denne publikasjonen i ny fane eller vindu >>Substance P Enhances Keratocyte Migration and Neutrophil Recruitment through Interleukin-8
2016 (engelsk)Inngår i: Molecular Pharmacology, ISSN 0026-895X, E-ISSN 1521-0111, Vol. 89, nr 2, s. 215-225Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Keratocytes, the resident cells of the corneal stroma, are responsible for maintaining turnover of this tissue by synthesizing extracellular matrix components. When the cornea is injured, the keratocytes migrate to the wounded site and participate in the stromal wound healing. The neuropeptide substance P (SP), which is also known to be produced by non-neuronal cells, has previously been implicated in epithelial wound healing after corneal injury. Corneal scarring, which occurs in the stroma when the process of wound healing has malfunctioned, is one of the major causes of preventable blindness. This study aimed to elucidate the potential role of SP in keratocyte migration and therefore in stromal wound healing. We report that the expression and secretion of SP in human keratocytes are increased in response to injury in vitro. Moreover, SP enhances the migration of keratocytes by inducing the actin cytoskeleton reorganization and focal adhesion formation through the activation of the phosphatidylinositide 3-kinase and Ras-related C3 botulinum toxin substrate 1/Ras homolog gene family, member A pathway. Furthermore, SP stimulation leads to upregulated expression of the proinflammatory and chemotactic cytokine interleukin-8 (IL-8), which also contributes significantly to SP-enhanced keratocyte migration and is able to attract neutrophils. In addition, the preferred SP receptor, the neurokinin-1 receptor, is necessary to induce keratocyte migration and IL-8 secretion. In conclusion, we describe new mechanisms by which SP enhances migration of keratocytes and recruits neutrophils, two necessary steps in the corneal wound-healing process, which are also likely to occur in other tissue injuries.

HSV kategori
Identifikatorer
urn:nbn:se:umu:diva-117400 (URN)10.1124/mol.115.101014 (DOI)000369305700001 ()26646648 (PubMedID)2-s2.0-84958149768 (Scopus ID)
Tilgjengelig fra: 2016-04-05 Laget: 2016-02-29 Sist oppdatert: 2023-03-24bibliografisk kontrollert
Organisasjoner
Identifikatorer
ORCID-id: ORCID iD iconorcid.org/0000-0002-8039-493x