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Erratum to: Plasma levels of matrix metalloproteinase-2, -3, -10, and tissue inhibitor of metalloproteinase-1 are associated with vascular complications in patients with type 1 diabetes: the EURODIAB Prospective Complications Study.

Cardiovascular diabetology

Peeters SA, Engelen L, Buijs J, Chaturvedi N, Fuller JH, Schalkwijk CG, Stehouwer CD.
PMID: 26415611
Cardiovasc Diabetol. 2015 Sep 28;14:128. doi: 10.1186/s12933-015-0290-4.

No abstract available.

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Peeters SA, Engelen L, Buijs J, et al. Erratum to: Plasma levels of matrix metalloproteinase-2, -3, -10, and tissue inhibitor of metalloproteinase-1 are associated with vascular complications in patients with type 1 diabetes: the EURODIAB Prospective Complications Study. Cardiovasc Diabetol. 2015;14:128doi: 10.1186/s12933-015-0290-4.
Peeters, S. A., Engelen, L., Buijs, J., Chaturvedi, N., Fuller, J. H., Schalkwijk, C. G., Stehouwer, C. D. (2015). Erratum to: Plasma levels of matrix metalloproteinase-2, -3, -10, and tissue inhibitor of metalloproteinase-1 are associated with vascular complications in patients with type 1 diabetes: the EURODIAB Prospective Complications Study. Cardiovascular diabetology, 14128. https://doi.org/10.1186/s12933-015-0290-4
Peeters, Stijn A, et al. "Erratum to: Plasma levels of matrix metalloproteinase-2, -3, -10, and tissue inhibitor of metalloproteinase-1 are associated with vascular complications in patients with type 1 diabetes: the EURODIAB Prospective Complications Study." Cardiovascular diabetology vol. 14 (2015): 128. doi: https://doi.org/10.1186/s12933-015-0290-4
Peeters SA, Engelen L, Buijs J, Chaturvedi N, Fuller JH, Schalkwijk CG, Stehouwer CD. Erratum to: Plasma levels of matrix metalloproteinase-2, -3, -10, and tissue inhibitor of metalloproteinase-1 are associated with vascular complications in patients with type 1 diabetes: the EURODIAB Prospective Complications Study. Cardiovasc Diabetol. 2015 Sep 28;14:128. doi: 10.1186/s12933-015-0290-4. PMID: 26415611; PMCID: PMC4587827.
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Role of interleukin-1 and its antagonism of hepatic stellate cell proliferation and liver fibrosis in the Abcb4(-/-) mouse model.

World journal of hepatology

Reiter FP, Wimmer R, Wottke L, Artmann R, Nagel JM, Carranza MO, Mayr D, Rust C, Fickert P, Trauner M, Gerbes AL, Hohenester S, Denk GU.
PMID: 27004088
World J Hepatol. 2016 Mar 18;8(8):401-10. doi: 10.4254/wjh.v8.i8.401.

AIM: To study the interleukin-1 (IL-1) pathway as a therapeutic target for liver fibrosis in vitro and in vivo using the ATP-binding cassette transporter b4(-/-) (Abcb4(-/-)) mouse model.METHODS: Female and male Abcb4(-/-) mice from 6 to 13 mo of...

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Reiter FP, Wimmer R, Wottke L, et al. Role of interleukin-1 and its antagonism of hepatic stellate cell proliferation and liver fibrosis in the Abcb4(-/-) mouse model. World J Hepatol. 2016;8(8):401-10doi: 10.4254/wjh.v8.i8.401.
Reiter, F. P., Wimmer, R., Wottke, L., Artmann, R., Nagel, J. M., Carranza, M. O., Mayr, D., Rust, C., Fickert, P., Trauner, M., Gerbes, A. L., Hohenester, S., & Denk, G. U. (2016). Role of interleukin-1 and its antagonism of hepatic stellate cell proliferation and liver fibrosis in the Abcb4(-/-) mouse model. World journal of hepatology, 8(8), 401-10. https://doi.org/10.4254/wjh.v8.i8.401
Reiter, Florian P, et al. "Role of interleukin-1 and its antagonism of hepatic stellate cell proliferation and liver fibrosis in the Abcb4(-/-) mouse model." World journal of hepatology vol. 8,8 (2016): 401-10. doi: https://doi.org/10.4254/wjh.v8.i8.401
Reiter FP, Wimmer R, Wottke L, Artmann R, Nagel JM, Carranza MO, Mayr D, Rust C, Fickert P, Trauner M, Gerbes AL, Hohenester S, Denk GU. Role of interleukin-1 and its antagonism of hepatic stellate cell proliferation and liver fibrosis in the Abcb4(-/-) mouse model. World J Hepatol. 2016 Mar 18;8(8):401-10. doi: 10.4254/wjh.v8.i8.401. PMID: 27004088; PMCID: PMC4794530.
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Serum and tissue biomarkers in aortic stenosis.

Global cardiology science & practice

Kapelouzou A, Tsourelis L, Kaklamanis L, Degiannis D, Kogerakis N, Cokkinos DV.
PMID: 26779524
Glob Cardiol Sci Pract. 2015 Nov 13;2015(4):49. doi: 10.5339/gcsp.2015.49. eCollection 2015.

BACKGROUND: Calcific aortic valve stenosis (CAVS) is seen in a large proportion of individuals over 60 years. It is an active process, influenced by lipid accumulation, mechanical stress, inflammation, and abnormal extracellular matrix turnover. Various biomarkers (BMs) are studied,...

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Kapelouzou A, Tsourelis L, Kaklamanis L, et al. Serum and tissue biomarkers in aortic stenosis. Glob Cardiol Sci Pract. 2015;2015(4):49doi: 10.5339/gcsp.2015.49.
Kapelouzou, A., Tsourelis, L., Kaklamanis, L., Degiannis, D., Kogerakis, N., & Cokkinos, D. V. (2015). Serum and tissue biomarkers in aortic stenosis. Global cardiology science & practice, 2015(4), 49. https://doi.org/10.5339/gcsp.2015.49
Kapelouzou, Alkistis, et al. "Serum and tissue biomarkers in aortic stenosis." Global cardiology science & practice vol. 2015,4 (2015): 49. doi: https://doi.org/10.5339/gcsp.2015.49
Kapelouzou A, Tsourelis L, Kaklamanis L, Degiannis D, Kogerakis N, Cokkinos DV. Serum and tissue biomarkers in aortic stenosis. Glob Cardiol Sci Pract. 2015 Nov 13;2015(4):49. doi: 10.5339/gcsp.2015.49. eCollection 2015. PMID: 26779524; PMCID: PMC4710866.
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TUC338 promotes cell migration and invasion by targeting TIMP1 in cervical cancer.

Oncology letters

Li Q, Shen F, Wang C.
PMID: 28599453
Oncol Lett. 2017 Jun;13(6):4526-4532. doi: 10.3892/ol.2017.5971. Epub 2017 Apr 03.

Ultraconserved regions (UCRs) are non-protein-coding gene sequences that are strictly conserved across numerous distinct species. It has been demonstrated previously that UCRs encoding non-coding RNAs serve as regulators of gene expression. In recent decades, there has been increasing evidence...

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Li Q, Shen F, Wang C. TUC338 promotes cell migration and invasion by targeting TIMP1 in cervical cancer. Oncol Lett. 2017;13(6):4526-4532doi: 10.3892/ol.2017.5971.
Li, Q., Shen, F., & Wang, C. (2017). TUC338 promotes cell migration and invasion by targeting TIMP1 in cervical cancer. Oncology letters, 13(6), 4526-4532. https://doi.org/10.3892/ol.2017.5971
Li, Qin, et al. "TUC338 promotes cell migration and invasion by targeting TIMP1 in cervical cancer." Oncology letters vol. 13,6 (2017): 4526-4532. doi: https://doi.org/10.3892/ol.2017.5971
Li Q, Shen F, Wang C. TUC338 promotes cell migration and invasion by targeting TIMP1 in cervical cancer. Oncol Lett. 2017 Jun;13(6):4526-4532. doi: 10.3892/ol.2017.5971. Epub 2017 Apr 03. PMID: 28599453; PMCID: PMC5453013.
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The ERK1/2 Inhibitor U0126 Attenuates Diabetes-Induced Upregulation of MMP-9 and Biomarkers of Inflammation in the Retina.

Journal of diabetes research

Mohammad G, Mairaj Siddiquei M, Imtiaz Nawaz M, Abu El-Asrar AM.
PMID: 23671886
J Diabetes Res. 2013;2013:658548. doi: 10.1155/2013/658548. Epub 2013 Apr 10.

This study was conducted to determine the expression of matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of metalloproteinase-1 (TIMP-1) in a time-dependent manner and the effect of extracellular-signal-regulated kinases-1/2 (ERK1/2) inhibition on the expressions of MMP-9, TIMP-1, and inflammatory biomarkers...

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Mohammad G, Mairaj Siddiquei M, Imtiaz Nawaz M, et al. The ERK1/2 Inhibitor U0126 Attenuates Diabetes-Induced Upregulation of MMP-9 and Biomarkers of Inflammation in the Retina. J Diabetes Res. 2013;2013:658548doi: 10.1155/2013/658548.
Mohammad, G., Mairaj Siddiquei, M., Imtiaz Nawaz, M., & Abu El-Asrar, A. M. (2013). The ERK1/2 Inhibitor U0126 Attenuates Diabetes-Induced Upregulation of MMP-9 and Biomarkers of Inflammation in the Retina. Journal of diabetes research, 2013658548. https://doi.org/10.1155/2013/658548
Mohammad, Ghulam, et al. "The ERK1/2 Inhibitor U0126 Attenuates Diabetes-Induced Upregulation of MMP-9 and Biomarkers of Inflammation in the Retina." Journal of diabetes research vol. 2013 (2013): 658548. doi: https://doi.org/10.1155/2013/658548
Mohammad G, Mairaj Siddiquei M, Imtiaz Nawaz M, Abu El-Asrar AM. The ERK1/2 Inhibitor U0126 Attenuates Diabetes-Induced Upregulation of MMP-9 and Biomarkers of Inflammation in the Retina. J Diabetes Res. 2013;2013:658548. doi: 10.1155/2013/658548. Epub 2013 Apr 10. PMID: 23671886; PMCID: PMC3647581.
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Regenerating white matter using human iPSC-derived immature astroglia.

Neurogenesis (Austin, Tex.)

Jiang P, Deng W.
PMID: 27652287
Neurogenesis (Austin). 2016 Sep 08;3(1):e1224453. doi: 10.1080/23262133.2016.1224453. eCollection 2016.

Astrocytes traditionally were thought to have merely a support function, but are now understood to be important regulators of neural development and function. The immature and mature astrocytes have stage-specific roles in neuronal development. However, it is largely unclear...

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Jiang P, Deng W. Regenerating white matter using human iPSC-derived immature astroglia. Neurogenesis (Austin). 2016;3(1):e1224453doi: 10.1080/23262133.2016.1224453.
Jiang, P., & Deng, W. (2016). Regenerating white matter using human iPSC-derived immature astroglia. Neurogenesis (Austin, Tex.), 3(1), e1224453. https://doi.org/10.1080/23262133.2016.1224453
Jiang, Peng, and Deng, Wenbin. "Regenerating white matter using human iPSC-derived immature astroglia." Neurogenesis (Austin, Tex.) vol. 3,1 (2016): e1224453. doi: https://doi.org/10.1080/23262133.2016.1224453
Jiang P, Deng W. Regenerating white matter using human iPSC-derived immature astroglia. Neurogenesis (Austin). 2016 Sep 08;3(1):e1224453. doi: 10.1080/23262133.2016.1224453. eCollection 2016. PMID: 27652287; PMCID: PMC5026801.
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Cotreatment with interferon-alpha and -gamma reduces liver fibrosis in a rat model.

Hepatology research : the official journal of the Japan Society of Hepatology

Takahara T, Sugiyama K, Zhang LP, Ando O, Fujii M, Yata Y, Bo J, Xue F, Minemura M, Watanabe A.
PMID: 15036071
Hepatol Res. 2004 Mar;28(3):146-154. doi: 10.1016/j.hepres.2003.11.003.

Background/Aims: Interferon-alpha is used widely to treat viral hepatitis. Interferon-gamma modulates a system attacking infected cells and also has an anti-fibrotic effect. A treatment with interferon-alpha and -gamma has undergone trials in eliminating hepatitis C virus. We investigated effects...

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Takahara T, Sugiyama K, Zhang LP, et al. Cotreatment with interferon-alpha and -gamma reduces liver fibrosis in a rat model. Hepatol Res. 2004;28(3):146-154doi: 10.1016/j.hepres.2003.11.003.
Takahara, T., Sugiyama, K., Zhang, L. P., Ando, O., Fujii, M., Yata, Y., Bo, J., Xue, F., Minemura, M., & Watanabe, A. (2004). Cotreatment with interferon-alpha and -gamma reduces liver fibrosis in a rat model. Hepatology research : the official journal of the Japan Society of Hepatology, 28(3), 146-154. https://doi.org/10.1016/j.hepres.2003.11.003
Takahara, Terumi, et al. "Cotreatment with interferon-alpha and -gamma reduces liver fibrosis in a rat model." Hepatology research : the official journal of the Japan Society of Hepatology vol. 28,3 (2004): 146-154. doi: https://doi.org/10.1016/j.hepres.2003.11.003
Takahara T, Sugiyama K, Zhang LP, Ando O, Fujii M, Yata Y, Bo J, Xue F, Minemura M, Watanabe A. Cotreatment with interferon-alpha and -gamma reduces liver fibrosis in a rat model. Hepatol Res. 2004 Mar;28(3):146-154. doi: 10.1016/j.hepres.2003.11.003. PMID: 15036071.
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Amnion-derived cellular cytokine solution: a physiological combination of cytokines for wound healing.

Eplasty

Steed DL, Trumpower C, Duffy D, Smith C, Marshall V, Rupp R, Robson M.
PMID: 18461121
Eplasty. 2008 Apr 07;8:e18.

OBJECTIVE: Wound repair is a complex integration of dynamic processes mediated by humeral messages controlling the levels of cytokines, growth factors, and matrix metalloproteinases in the wound space. Isolated growth factors and growth factor combinations have been used to...

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Steed DL, Trumpower C, Duffy D, et al. Amnion-derived cellular cytokine solution: a physiological combination of cytokines for wound healing. Eplasty. 2008;8:e18
Steed, D. L., Trumpower, C., Duffy, D., Smith, C., Marshall, V., Rupp, R., & Robson, M. (2008). Amnion-derived cellular cytokine solution: a physiological combination of cytokines for wound healing. Eplasty, 8e18.
Steed, David L, et al. "Amnion-derived cellular cytokine solution: a physiological combination of cytokines for wound healing." Eplasty vol. 8 (2008): e18.
Steed DL, Trumpower C, Duffy D, Smith C, Marshall V, Rupp R, Robson M. Amnion-derived cellular cytokine solution: a physiological combination of cytokines for wound healing. Eplasty. 2008 Apr 07;8:e18. PMID: 18461121; PMCID: PMC2311453.
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Wound fluids from saline solution- and Staphylococcus aureus peptidoglycan-inoculated sponges induce expression of matrix metalloproteinase 13 messenger ribonucleic acid by cultured rat fibroblasts.

Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society

Liu X, Chang TH, Rojkind M, Levenson SM.
PMID: 16984445
Wound Repair Regen. 1997 Oct-Dec;5(4):348-54. doi: 10.1046/j.1524-475x.1997.t01-1-50409.x.

Polyvinyl alcohol sponges inoculated with Staphylococcus aureus peptidoglycan induce an accelerated wound healing response when implanted subcutaneously in rats. S. aureus peptidoglycan leads to a marked increase (50%) in reparative tissue collagen (as measured by hydroxyproline) by 4 days....

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Liu X, Chang TH, Rojkind M, et al. Wound fluids from saline solution- and Staphylococcus aureus peptidoglycan-inoculated sponges induce expression of matrix metalloproteinase 13 messenger ribonucleic acid by cultured rat fibroblasts. Wound Repair Regen. 1997;5(4):348-54doi: 10.1046/j.1524-475x.1997.t01-1-50409.x.
Liu, X., Chang, T. H., Rojkind, M., & Levenson, S. M. (1997). Wound fluids from saline solution- and Staphylococcus aureus peptidoglycan-inoculated sponges induce expression of matrix metalloproteinase 13 messenger ribonucleic acid by cultured rat fibroblasts. Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society, 5(4), 348-54. https://doi.org/10.1046/j.1524-475x.1997.t01-1-50409.x
Liu, X, et al. "Wound fluids from saline solution- and Staphylococcus aureus peptidoglycan-inoculated sponges induce expression of matrix metalloproteinase 13 messenger ribonucleic acid by cultured rat fibroblasts." Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society vol. 5,4 (1997): 348-54. doi: https://doi.org/10.1046/j.1524-475x.1997.t01-1-50409.x
Liu X, Chang TH, Rojkind M, Levenson SM. Wound fluids from saline solution- and Staphylococcus aureus peptidoglycan-inoculated sponges induce expression of matrix metalloproteinase 13 messenger ribonucleic acid by cultured rat fibroblasts. Wound Repair Regen. 1997 Oct-Dec;5(4):348-54. doi: 10.1046/j.1524-475x.1997.t01-1-50409.x. PMID: 16984445.
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Role of angiogenic factors in airway remodeling in an allergic rhinitis murine model.

Allergy, asthma & immunology research

Moon IJ, Kim DY, Rhee CS, Lee CH, Min YG.
PMID: 22211169
Allergy Asthma Immunol Res. 2012 Jan;4(1):37-45. doi: 10.4168/aair.2012.4.1.37. Epub 2011 Nov 01.

PURPOSE: There is growing evidence that nasal airway remodeling occurs in allergic rhinitis (AR). Although angiogenesis is an important component of airway remodeling in asthma, its involvement in AR has been little studied. Furthermore, information regarding the role of...

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Moon IJ, Kim DY, Rhee CS, et al. Role of angiogenic factors in airway remodeling in an allergic rhinitis murine model. Allergy Asthma Immunol Res. 2011;4(1):37-45doi: 10.4168/aair.2012.4.1.37.
Moon, I. J., Kim, D. Y., Rhee, C. S., Lee, C. H., & Min, Y. G. (2012). Role of angiogenic factors in airway remodeling in an allergic rhinitis murine model. Allergy, asthma & immunology research, 4(1), 37-45. https://doi.org/10.4168/aair.2012.4.1.37
Moon, Il Joon, et al. "Role of angiogenic factors in airway remodeling in an allergic rhinitis murine model." Allergy, asthma & immunology research vol. 4,1 (2012): 37-45. doi: https://doi.org/10.4168/aair.2012.4.1.37
Moon IJ, Kim DY, Rhee CS, Lee CH, Min YG. Role of angiogenic factors in airway remodeling in an allergic rhinitis murine model. Allergy Asthma Immunol Res. 2012 Jan;4(1):37-45. doi: 10.4168/aair.2012.4.1.37. Epub 2011 Nov 01. PMID: 22211169; PMCID: PMC3242059.
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The role of interleukin 17 in Crohn's disease-associated intestinal fibrosis.

Fibrogenesis & tissue repair

Biancheri P, Pender SL, Ammoscato F, Giuffrida P, Sampietro G, Ardizzone S, Ghanbari A, Curciarello R, Pasini A, Monteleone G, Corazza GR, Macdonald TT, Di Sabatino A.
PMID: 23834907
Fibrogenesis Tissue Repair. 2013 Jul 08;6(1):13. doi: 10.1186/1755-1536-6-13.

BACKGROUND: Interleukin (IL)-17A and IL-17E (also known as IL-25) have been implicated in fibrosis in various tissues. However, the role of these cytokines in the development of intestinal strictures in Crohn's disease (CD) has not been explored. We investigated...

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Biancheri P, Pender SL, Ammoscato F, et al. The role of interleukin 17 in Crohn's disease-associated intestinal fibrosis. Fibrogenesis Tissue Repair. 2013;6(1):13doi: 10.1186/1755-1536-6-13.
Biancheri, P., Pender, S. L., Ammoscato, F., Giuffrida, P., Sampietro, G., Ardizzone, S., Ghanbari, A., Curciarello, R., Pasini, A., Monteleone, G., Corazza, G. R., Macdonald, T. T., & Di Sabatino, A. (2013). The role of interleukin 17 in Crohn's disease-associated intestinal fibrosis. Fibrogenesis & tissue repair, 6(1), 13. https://doi.org/10.1186/1755-1536-6-13
Biancheri, Paolo, et al. "The role of interleukin 17 in Crohn's disease-associated intestinal fibrosis." Fibrogenesis & tissue repair vol. 6,1 (2013): 13. doi: https://doi.org/10.1186/1755-1536-6-13
Biancheri P, Pender SL, Ammoscato F, Giuffrida P, Sampietro G, Ardizzone S, Ghanbari A, Curciarello R, Pasini A, Monteleone G, Corazza GR, Macdonald TT, Di Sabatino A. The role of interleukin 17 in Crohn's disease-associated intestinal fibrosis. Fibrogenesis Tissue Repair. 2013 Jul 08;6(1):13. doi: 10.1186/1755-1536-6-13. PMID: 23834907; PMCID: PMC3733737.
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The α(1)AT and TIMP-1 Gene Polymorphism in the Development of Asthma.

Comparative and functional genomics

Kumar M, Bhadoria DP, Dutta K, Kumar F M, Singh B, Singh S, Chhillar AK, Behera D, Sharma GL.
PMID: 23226977
Comp Funct Genomics. 2012;2012:968267. doi: 10.1155/2012/968267. Epub 2012 Nov 21.

Asthma has been an inflammatory disorder accompanied by tissue remodeling and protease-antiprotease imbalance in lungs. The SNPs of alpha-1 antitrypsin (α(1)AT) and tissue inhibitor of metalloproteinase-1 (TIMP-1) genes were studied for their association with asthma. Genotyping of α(1)AT and...

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Kumar M, Bhadoria DP, Dutta K, et al. The α(1)AT and TIMP-1 Gene Polymorphism in the Development of Asthma. Comp Funct Genomics. 2012;2012:968267doi: 10.1155/2012/968267.
Kumar, M., Bhadoria, D. P., Dutta, K., Kumar F, M., Singh, B., Singh, S., Chhillar, A. K., Behera, D., & Sharma, G. L. (2012). The α(1)AT and TIMP-1 Gene Polymorphism in the Development of Asthma. Comparative and functional genomics, 2012968267. https://doi.org/10.1155/2012/968267
Kumar, Manish, et al. "The α(1)AT and TIMP-1 Gene Polymorphism in the Development of Asthma." Comparative and functional genomics vol. 2012 (2012): 968267. doi: https://doi.org/10.1155/2012/968267
Kumar M, Bhadoria DP, Dutta K, Kumar F M, Singh B, Singh S, Chhillar AK, Behera D, Sharma GL. The α(1)AT and TIMP-1 Gene Polymorphism in the Development of Asthma. Comp Funct Genomics. 2012;2012:968267. doi: 10.1155/2012/968267. Epub 2012 Nov 21. PMID: 23226977; PMCID: PMC3512250.
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