Effect of Matrix Metallopeptidase 13 on the Function of Mouse Bone Marrow-derived Dendritic Cells
Background: Dendritic cells are professional antigen-presenting cells found in an immature state in epithelia and interstitial space, where they capture antigens such as pathogens or damaged tissue. Matrix metallopeptidase 13 (MMP- 13), a member of the collagenase subfamily, is involved in many diff...
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Published in | Chinese medical journal Vol. 130; no. 6; pp. 717 - 721 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
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China
Medknow Publications and Media Pvt. Ltd
20.03.2017
Lippincott Williams & Wilkins Ovid Technologies Department of Dermatology, Central Hospital Affiliated to Shenyang Medical College, Shenyang, Liaoning 110024, China%Department of Dermatology Key Laboratory of Immunodermatology, No.1 Hospital of China Medical University, Shenyang, Liaoning 110001, China%Department of Oncology, Central Hospital Affiliated to Shenyang Medical College, Shenyang, Liaoning 110024, China Medknow Publications & Media Pvt Ltd Wolters Kluwer |
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Abstract | Background: Dendritic cells are professional antigen-presenting cells found in an immature state in epithelia and interstitial space, where they capture antigens such as pathogens or damaged tissue. Matrix metallopeptidase 13 (MMP- 13), a member of the collagenase subfamily, is involved in many different cellular processes and is expressed in murine bone marrow-derived dendritic cells (DCs). The function of MMP-13 in DCs is not well understood. Here, we investigated the effect of MMP-13 on DC maturation, apoptosis, and phagocytosis. Methods: Bone marrow-derived dendritic cells were obtained fiom C57BL/6 mice. One short-interfering RNA specific for MMP- 13 was used to transfect DCs. MMP-13-silenced DCs and control DCs were prepared, and apoptosis was measured using real-time polymerase chain reaction and Western blotting. MMP-13-silenced DCs and control DCs were analyzed for surface expression of CD80 and CD86 and phagocytosis capability using flow cytometry. Results: Compared to the control DCs, MMP- 13-silenced DCs increased expression of anti-apoptosis-related genes, BAGl (control group vs. MMP-13-silenced group: 4.08 ± 0.60 vs. 6.11 ± 0.87, P = 0.008), BCL-2 (control group vs. MMP-13-silenced group: 7.54 ± 0.76 vs. 9.54 ± 1.29, P = 0.036), and TP73 (control group vs. MMP- 13-silenced group: 4.33 ± 0.29 vs. 5.60 ±0.32, P = 0.001 ) and decreased apoptosis-related genes, CASPI (control group vs. MMP- 13-silenced group: 3.79±0.67 vs. 2.54±0.39, P - 0.019), LTBR (control group vs. MMP- 13-silenced group: 9.23 ±1.25 vs. 6.24 ± 1.15, P = 0.012), and CASP4 (control group vs. MMP-13-silenced group: 2.07 ± 0.56 vs. 0.35 ±0.35, P = 0.002). Protein levels confirmed the same expression pattern. MMP- 13-silenced groups decreased expression of CD86 on DCs; however, there was no statistical difference in CD80 surface expression. Furthermore, MMP-13-silenced groups exhibited weaker phagocytosis capability. Conclusion: These results indicate that MMP-13 inhibition dampens DC maturation, apoptosis, and phagocytosis. |
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AbstractList | Background:Dendritic cells are professional antigen-presenting ceils found in an immature state in epithelia and interstitial space,where they capture antigens such as pathogens or damaged tissue.Matrix metallopeptidase 13 (MMP-13),a member of the collagenase subfamily,is involved in many different cellular processes and is expressed in murine bone marrow-derived dendritic cells (DCs).The function of MMP-13 in DCs is not well understood.Here,we investigated the effect of MMP-13 on DC maturation,apoptosis,and phagocytosis.Methods:Bone marrow-derived dendritic cells were obtained from C57BL/6 mice.One short-interfering RNA specific for MMP-13 was used to transfect DCs.MMP-13-silenced DCs and control DCs were prepared,and apoptosis was measured using real-time polymerase chain reaction and Western blotting.MMP-13-silenced DCs and control DCs were analyzed for surface expression of CD80 and CD86 and phagocytosis capability using flow cytometry.Results:Compared to the control DCs,MMP-13-silenced DCs increased expression ofanti-apoptosis-related genes,BAG1 (control group vs.MMP-13-silenced group:4.08 ± 0.60 vs.6.11 ± 0.87,P =0.008),BCL-2 (control group vs.MMP-13-silenced group:7.54 ± 0.76 vs.9.54 ±1.29,P =0.036),and TP73 (control group vs.MMP-13-silenced group:4.33 ± 0.29 vs.5.60 ± 0.32,P =0.001) and decreased apoptosis-related genes,CASP1 (control group vs.MMP-13-silenced group:3.79 ± 0.67 vs.2.54 ± 0.39,P =0.019),LTBR (control group vs.MMP-13-silenced group:9.23 ± 1.25 vs.6.24 ± 1.15,P =0.012),and CASP4 (control group vs.MMP-13-silenced group:2.07 ± 0.56 vs.0.35 ± 0.35,P =0.002).Protein levels confirmed the same expression pattern.MMP-13-silenced groups decreased expression of CD86 on DCs;however,there was no statistical difference in CD80 surface expression.Furthermore,MMP-13-silenced groups exhibited weaker phagocytosis capability.Conclusion:These results indicate that MMP-13 inhibition dampens DC maturation,apoptosis,and phagocytosis. BACKGROUNDDendritic cells are professional antigen-presenting cells found in an immature state in epithelia and interstitial space, where they capture antigens such as pathogens or damaged tissue. Matrix metallopeptidase 13 (MMP-13), a member of the collagenase subfamily, is involved in many different cellular processes and is expressed in murine bone marrow-derived dendritic cells (DCs). The function of MMP-13 in DCs is not well understood. Here, we investigated the effect of MMP-13 on DC maturation, apoptosis, and phagocytosis.METHODSBone marrow-derived dendritic cells were obtained from C57BL/6 mice. One short-interfering RNA specific for MMP-13 was used to transfect DCs. MMP-13-silenced DCs and control DCs were prepared, and apoptosis was measured using real-time polymerase chain reaction and Western blotting. MMP-13-silenced DCs and control DCs were analyzed for surface expression of CD80 and CD86 and phagocytosis capability using flow cytometry.RESULTSCompared to the control DCs, MMP-13-silenced DCs increased expression of anti-apoptosis-related genes, BAG1 (control group vs. MMP-13-silenced group: 4.08 ± 0.60 vs. 6.11 ± 0.87, P = 0.008), BCL-2 (control group vs. MMP-13-silenced group: 7.54 ± 0.76 vs. 9.54 ± 1.29, P = 0.036), and TP73 (control group vs. MMP-13-silenced group: 4.33 ± 0.29 vs. 5.60 ± 0.32, P = 0.001) and decreased apoptosis-related genes, CASP1 (control group vs. MMP-13-silenced group: 3.79 ± 0.67 vs. 2.54 ± 0.39, P = 0.019), LTBR (control group vs. MMP-13-silenced group: 9.23 ± 1.25 vs. 6.24 ± 1.15, P = 0.012), and CASP4 (control group vs. MMP-13-silenced group: 2.07 ± 0.56 vs. 0.35 ± 0.35, P = 0.002). Protein levels confirmed the same expression pattern. MMP-13-silenced groups decreased expression of CD86 on DCs; however, there was no statistical difference in CD80 surface expression. Furthermore, MMP-13-silenced groups exhibited weaker phagocytosis capability.CONCLUSIONThese results indicate that MMP-13 inhibition dampens DC maturation, apoptosis, and phagocytosis. Background: Dendritic cells are professional antigen-presenting cells found in an immature state in epithelia and interstitial space, where they capture antigens such as pathogens or damaged tissue. Matrix metallopeptidase 13 (MMP- 13), a member of the collagenase subfamily, is involved in many different cellular processes and is expressed in murine bone marrow-derived dendritic cells (DCs). The function of MMP-13 in DCs is not well understood. Here, we investigated the effect of MMP-13 on DC maturation, apoptosis, and phagocytosis. Methods: Bone marrow-derived dendritic cells were obtained fiom C57BL/6 mice. One short-interfering RNA specific for MMP- 13 was used to transfect DCs. MMP-13-silenced DCs and control DCs were prepared, and apoptosis was measured using real-time polymerase chain reaction and Western blotting. MMP-13-silenced DCs and control DCs were analyzed for surface expression of CD80 and CD86 and phagocytosis capability using flow cytometry. Results: Compared to the control DCs, MMP- 13-silenced DCs increased expression of anti-apoptosis-related genes, BAGl (control group vs. MMP-13-silenced group: 4.08 ± 0.60 vs. 6.11 ± 0.87, P = 0.008), BCL-2 (control group vs. MMP-13-silenced group: 7.54 ± 0.76 vs. 9.54 ± 1.29, P = 0.036), and TP73 (control group vs. MMP- 13-silenced group: 4.33 ± 0.29 vs. 5.60 ±0.32, P = 0.001 ) and decreased apoptosis-related genes, CASPI (control group vs. MMP- 13-silenced group: 3.79±0.67 vs. 2.54±0.39, P - 0.019), LTBR (control group vs. MMP- 13-silenced group: 9.23 ±1.25 vs. 6.24 ± 1.15, P = 0.012), and CASP4 (control group vs. MMP-13-silenced group: 2.07 ± 0.56 vs. 0.35 ±0.35, P = 0.002). Protein levels confirmed the same expression pattern. MMP- 13-silenced groups decreased expression of CD86 on DCs; however, there was no statistical difference in CD80 surface expression. Furthermore, MMP-13-silenced groups exhibited weaker phagocytosis capability. Conclusion: These results indicate that MMP-13 inhibition dampens DC maturation, apoptosis, and phagocytosis. Background: Dendritic cells are professional antigen-presenting cells found in an immature state in epithelia and interstitial space, where they capture antigens such as pathogens or damaged tissue. Matrix metallopeptidase 13 (MMP-13), a member of the collagenase subfamily, is involved in many different cellular processes and is expressed in murine bone marrow-derived dendritic cells (DCs). The function of MMP-13 in DCs is not well understood. Here, we investigated the effect of MMP-13 on DC maturation, apoptosis, and phagocytosis. Methods: Bone marrow-derived dendritic cells were obtained from C57BL/6 mice. One short-interfering RNA specific for MMP-13 was used to transfect DCs. MMP-13-silenced DCs and control DCs were prepared, and apoptosis was measured using real-time polymerase chain reaction and Western blotting. MMP-13-silenced DCs and control DCs were analyzed for surface expression of CD80 and CD86 and phagocytosis capability using flow cytometry. Results: Compared to the control DCs, MMP-13-silenced DCs increased expression of anti-apoptosis-related genes, BAG1 (control group vs. MMP-13-silenced group: 4.08 ± 0.60 vs. 6.11 ± 0.87, P = 0.008), BCL-2 (control group vs. MMP-13-silenced group: 7.54 ± 0.76 vs. 9.54 ± 1.29, P = 0.036), and TP73 (control group vs. MMP-13-silenced group: 4.33 ± 0.29 vs. 5.60 ± 0.32, P = 0.001) and decreased apoptosis-related genes, CASP1 (control group vs. MMP-13-silenced group: 3.79 ± 0.67 vs. 2.54 ± 0.39, P = 0.019), LTBR (control group vs. MMP-13-silenced group: 9.23 ± 1.25 vs. 6.24 ± 1.15, P = 0.012), and CASP4 (control group vs. MMP-13-silenced group: 2.07 ± 0.56 vs. 0.35 ± 0.35, P = 0.002). Protein levels confirmed the same expression pattern. MMP-13-silenced groups decreased expression of CD86 on DCs; however, there was no statistical difference in CD80 surface expression. Furthermore, MMP-13-silenced groups exhibited weaker phagocytosis capability. Conclusion: These results indicate that MMP-13 inhibition dampens DC maturation, apoptosis, and phagocytosis. Dendritic cells are professional antigen-presenting cells found in an immature state in epithelia and interstitial space, where they capture antigens such as pathogens or damaged tissue. Matrix metallopeptidase 13 (MMP-13), a member of the collagenase subfamily, is involved in many different cellular processes and is expressed in murine bone marrow-derived dendritic cells (DCs). The function of MMP-13 in DCs is not well understood. Here, we investigated the effect of MMP-13 on DC maturation, apoptosis, and phagocytosis. Bone marrow-derived dendritic cells were obtained from C57BL/6 mice. One short-interfering RNA specific for MMP-13 was used to transfect DCs. MMP-13-silenced DCs and control DCs were prepared, and apoptosis was measured using real-time polymerase chain reaction and Western blotting. MMP-13-silenced DCs and control DCs were analyzed for surface expression of CD80 and CD86 and phagocytosis capability using flow cytometry. Compared to the control DCs, MMP-13-silenced DCs increased expression of anti-apoptosis-related genes, BAG1 (control group vs. MMP-13-silenced group: 4.08 ± 0.60 vs. 6.11 ± 0.87, P = 0.008), BCL-2 (control group vs. MMP-13-silenced group: 7.54 ± 0.76 vs. 9.54 ± 1.29, P = 0.036), and TP73 (control group vs. MMP-13-silenced group: 4.33 ± 0.29 vs. 5.60 ± 0.32, P = 0.001) and decreased apoptosis-related genes, CASP1 (control group vs. MMP-13-silenced group: 3.79 ± 0.67 vs. 2.54 ± 0.39, P = 0.019), LTBR (control group vs. MMP-13-silenced group: 9.23 ± 1.25 vs. 6.24 ± 1.15, P = 0.012), and CASP4 (control group vs. MMP-13-silenced group: 2.07 ± 0.56 vs. 0.35 ± 0.35, P = 0.002). Protein levels confirmed the same expression pattern. MMP-13-silenced groups decreased expression of CD86 on DCs; however, there was no statistical difference in CD80 surface expression. Furthermore, MMP-13-silenced groups exhibited weaker phagocytosis capability. These results indicate that MMP-13 inhibition dampens DC maturation, apoptosis, and phagocytosis. Background: Dendritic cells are professional antigen-presenting cells found in an immature state in epithelia and interstitial space, where they capture antigens such as pathogens or damaged tissue. Matrix metallopeptidase 13 (MMP-13), a member of the collagenase subfamily, is involved in many different cellular processes and is expressed in murine bone marrow-derived dendritic cells (DCs). The function of MMP-13 in DCs is not well understood. Here, we investigated the effect of MMP-13 on DC maturation, apoptosis, and phagocytosis. Methods: Bone marrow-derived dendritic cells were obtained from C57BL/6 mice. One short-interfering RNA specific for MMP-13 was used to transfect DCs. MMP-13-silenced DCs and control DCs were prepared, and apoptosis was measured using real-time polymerase chain reaction and Western blotting. MMP-13-silenced DCs and control DCs were analyzed for surface expression of CD80 and CD86 and phagocytosis capability using flow cytometry. Results: Compared to the control DCs, MMP-13-silenced DCs increased expression of anti-apoptosis-related genes, BAG1 (control group vs. MMP-13-silenced group: 4.08 +- 0.60 vs. 6.11 +- 0.87, P = 0.008), BCL-2 (control group vs. MMP-13-silenced group: 7.54 +- 0.76 vs. 9.54 +- 1.29, P = 0.036), and TP73 (control group vs. MMP-13-silenced group: 4.33 +- 0.29 vs. 5.60 +- 0.32, P = 0.001) and decreased apoptosis-related genes, CASP1 (control group vs. MMP-13-silenced group: 3.79 +- 0.67 vs. 2.54 +- 0.39, P = 0.019), LTBR (control group vs. MMP-13-silenced group: 9.23 +- 1.25 vs. 6.24 +- 1.15, P = 0.012), and CASP4 (control group vs. MMP-13-silenced group: 2.07 +- 0.56 vs. 0.35 +- 0.35, P = 0.002). Protein levels confirmed the same expression pattern. MMP-13-silenced groups decreased expression of CD86 on DCs; however, there was no statistical difference in CD80 surface expression. Furthermore, MMP-13-silenced groups exhibited weaker phagocytosis capability. Conclusion: These results indicate that MMP-13 inhibition dampens DC maturation, apoptosis, and phagocytosis. |
Audience | Academic |
Author | Xiao-Dong Li Xin-Rui Zhang Zhi-Hao Li Yang Yang Duo Zhang Heng Zheng Shu-Ying Dong Juan Chen Xian-Dong Zeng |
AuthorAffiliation | Department of Dermatology, Central Hospital Affiliated to Shenyang Medical College, Shenyang, Liaoning 110024, China Department of Dermatology Key Laboratory of Immunodermatology, No. 1 Hospital of China Medical University, Shenyang, Liaoning 110001, China Department of Oncology, Central Hospital Affiliated to Shenyang Medical College, Shenyang, Liaoning 110024, China |
AuthorAffiliation_xml | – name: Department of Dermatology, Central Hospital Affiliated to Shenyang Medical College, Shenyang, Liaoning 110024, China%Department of Dermatology Key Laboratory of Immunodermatology, No.1 Hospital of China Medical University, Shenyang, Liaoning 110001, China%Department of Oncology, Central Hospital Affiliated to Shenyang Medical College, Shenyang, Liaoning 110024, China – name: 2 Department of Dermatology Key Laboratory of Immunodermatology, No. 1 Hospital of China Medical University, Shenyang, Liaoning 110001, China – name: 3 Department of Oncology, Central Hospital Affiliated to Shenyang Medical College, Shenyang, Liaoning 110024, China – name: 1 Department of Dermatology, Central Hospital Affiliated to Shenyang Medical College, Shenyang, Liaoning 110024, China |
Author_xml | – sequence: 1 givenname: Xiao-Dong surname: Li fullname: Li, Xiao-Dong organization: Department of Dermatology, Central Hospital Affiliated to Shenyang Medical College, Shenyang, Liaoning 110024, China – sequence: 2 givenname: Xin-Rui surname: Zhang fullname: Zhang, Xin-Rui organization: Department of Dermatology, Central Hospital Affiliated to Shenyang Medical College, Shenyang, Liaoning 110024, China – sequence: 3 givenname: Zhi-Hao surname: Li fullname: Li, Zhi-Hao organization: Department of Dermatology, Central Hospital Affiliated to Shenyang Medical College, Shenyang, Liaoning 110024, China – sequence: 4 givenname: Yang surname: Yang fullname: Yang, Yang organization: Department of Dermatology Key Laboratory of Immunodermatology, No. 1 Hospital of China Medical University, Shenyang, Liaoning 110001, China – sequence: 5 givenname: Duo surname: Zhang fullname: Zhang, Duo organization: Department of Dermatology, Central Hospital Affiliated to Shenyang Medical College, Shenyang, Liaoning 110024, China – sequence: 6 givenname: Heng surname: Zheng fullname: Zheng, Heng organization: Department of Dermatology, Central Hospital Affiliated to Shenyang Medical College, Shenyang, Liaoning 110024, China – sequence: 7 givenname: Shu-Ying surname: Dong fullname: Dong, Shu-Ying organization: Department of Dermatology, Central Hospital Affiliated to Shenyang Medical College, Shenyang, Liaoning 110024, China – sequence: 8 givenname: Juan surname: Chen fullname: Chen, Juan organization: Department of Dermatology, Central Hospital Affiliated to Shenyang Medical College, Shenyang, Liaoning 110024, China – sequence: 9 givenname: Xian-Dong surname: Zeng fullname: Zeng, Xian-Dong organization: Department of Oncology, Central Hospital Affiliated to Shenyang Medical College, Shenyang, Liaoning 110024, China |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/28303856$$D View this record in MEDLINE/PubMed |
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CitedBy_id | crossref_primary_10_3390_pathogens10050527 crossref_primary_10_1016_j_aquaculture_2018_08_033 crossref_primary_10_1186_s12935_023_03116_0 |
Cites_doi | 10.1080/10409230290771483 10.1016/0003-4975(90)90248-5 10.1371/journal.pone.0042596 10.1111/j.1365-2249.2005.02840.x 10.1016/j.bbagen.2014.03.007 10.1016/j.semcdb.2007.07.003 10.1152/ajpcell.00051.2013 10.1038/nri1418 10.1006/bbrc.2001.6147 10.3109/15419069809004472 10.1136/thx.2008.104067 10.1016/j.acthis.2012.11.003 10.1242/jcs.00831 10.1093/intimm/dxw008 10.1111/exd.12722 10.3389/fimmu.2015.00133 |
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DocumentTitleAlternate | Effect of Matrix Metallopeptidase 13 on the Function of Mouse Bone Marrow-derived Dendritic Cells |
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Keywords | Matrix Metallopeptidase 13 Maturation Phagocytosis Dendritic Cell Apoptosis |
Language | English |
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Notes | Background: Dendritic cells are professional antigen-presenting cells found in an immature state in epithelia and interstitial space, where they capture antigens such as pathogens or damaged tissue. Matrix metallopeptidase 13 (MMP- 13), a member of the collagenase subfamily, is involved in many different cellular processes and is expressed in murine bone marrow-derived dendritic cells (DCs). The function of MMP-13 in DCs is not well understood. Here, we investigated the effect of MMP-13 on DC maturation, apoptosis, and phagocytosis. Methods: Bone marrow-derived dendritic cells were obtained fiom C57BL/6 mice. One short-interfering RNA specific for MMP- 13 was used to transfect DCs. MMP-13-silenced DCs and control DCs were prepared, and apoptosis was measured using real-time polymerase chain reaction and Western blotting. MMP-13-silenced DCs and control DCs were analyzed for surface expression of CD80 and CD86 and phagocytosis capability using flow cytometry. Results: Compared to the control DCs, MMP- 13-silenced DCs increased expression of anti-apoptosis-related genes, BAGl (control group vs. MMP-13-silenced group: 4.08 ± 0.60 vs. 6.11 ± 0.87, P = 0.008), BCL-2 (control group vs. MMP-13-silenced group: 7.54 ± 0.76 vs. 9.54 ± 1.29, P = 0.036), and TP73 (control group vs. MMP- 13-silenced group: 4.33 ± 0.29 vs. 5.60 ±0.32, P = 0.001 ) and decreased apoptosis-related genes, CASPI (control group vs. MMP- 13-silenced group: 3.79±0.67 vs. 2.54±0.39, P - 0.019), LTBR (control group vs. MMP- 13-silenced group: 9.23 ±1.25 vs. 6.24 ± 1.15, P = 0.012), and CASP4 (control group vs. MMP-13-silenced group: 2.07 ± 0.56 vs. 0.35 ±0.35, P = 0.002). Protein levels confirmed the same expression pattern. MMP- 13-silenced groups decreased expression of CD86 on DCs; however, there was no statistical difference in CD80 surface expression. Furthermore, MMP-13-silenced groups exhibited weaker phagocytosis capability. Conclusion: These results indicate that MMP-13 inhibition dampens DC maturation, apoptosis, and phagocytosis. Apoptosis; Dendritic Cell; Matrix Metallopeptidase 13: Maturation: Phagocytosis 11-2154/R ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
OpenAccessLink | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5358423/ |
PMID | 28303856 |
PQID | 1925227671 |
PQPubID | 2042885 |
PageCount | 5 |
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PublicationCentury | 2000 |
PublicationDate | 2017-03-20 |
PublicationDateYYYYMMDD | 2017-03-20 |
PublicationDate_xml | – month: 03 year: 2017 text: 2017-03-20 day: 20 |
PublicationDecade | 2010 |
PublicationPlace | China |
PublicationPlace_xml | – name: China – name: Baltimore – name: India |
PublicationTitle | Chinese medical journal |
PublicationTitleAlternate | Chinese Medical Journal |
PublicationTitle_FL | Chinese Medical Journal |
PublicationYear | 2017 |
Publisher | Medknow Publications and Media Pvt. Ltd Lippincott Williams & Wilkins Ovid Technologies Department of Dermatology, Central Hospital Affiliated to Shenyang Medical College, Shenyang, Liaoning 110024, China%Department of Dermatology Key Laboratory of Immunodermatology, No.1 Hospital of China Medical University, Shenyang, Liaoning 110001, China%Department of Oncology, Central Hospital Affiliated to Shenyang Medical College, Shenyang, Liaoning 110024, China Medknow Publications & Media Pvt Ltd Wolters Kluwer |
Publisher_xml | – name: Medknow Publications and Media Pvt. Ltd – name: Lippincott Williams & Wilkins Ovid Technologies – name: Department of Dermatology, Central Hospital Affiliated to Shenyang Medical College, Shenyang, Liaoning 110024, China%Department of Dermatology Key Laboratory of Immunodermatology, No.1 Hospital of China Medical University, Shenyang, Liaoning 110001, China%Department of Oncology, Central Hospital Affiliated to Shenyang Medical College, Shenyang, Liaoning 110024, China – name: Medknow Publications & Media Pvt Ltd – name: Wolters Kluwer |
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Snippet | Background: Dendritic cells are professional antigen-presenting cells found in an immature state in epithelia and interstitial space, where they capture... Dendritic cells are professional antigen-presenting cells found in an immature state in epithelia and interstitial space, where they capture antigens such as... Background: Dendritic cells are professional antigen-presenting cells found in an immature state in epithelia and interstitial space, where they capture... BACKGROUNDDendritic cells are professional antigen-presenting cells found in an immature state in epithelia and interstitial space, where they capture antigens... Background:Dendritic cells are professional antigen-presenting ceils found in an immature state in epithelia and interstitial space,where they capture antigens... |
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SubjectTerms | Animals Apoptosis Apoptosis - drug effects Apoptosis - physiology Apoptosis; Dendritic Cell; Matrix Metallopeptidase 13; Maturation; Phagocytosis Bone marrow Bone Marrow Cells - cytology DCS控制系统 Dendritic cells Dendritic Cells - cytology Dendritic Cells - drug effects Dendritic Cells - metabolism Dermatology Experiments Female Flow cytometry Gene expression Health aspects Hospitals Immunoglobulins Inflammation Lipopolysaccharides - pharmacology Matrix Metalloproteinase 13 - metabolism Matrix Metalloproteinase 13 - physiology Matrix metalloproteinase inhibitors Medical research Mice Mice, Inbred C57BL Original Polymerase chain reaction Proteins RNA, Small Interfering Western印迹法 凋亡相关基因 基质金属蛋白酶 小鼠骨髓 抗原呈递细胞 树突状细胞 细胞功能 |
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Title | Effect of Matrix Metallopeptidase 13 on the Function of Mouse Bone Marrow-derived Dendritic Cells |
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