Escherichia coli induced matrix metalloproteinase-9 activity and type IV collagen degradation is regulated by progesterone in human maternal decidual.


Journal

BMC pregnancy and childbirth
ISSN: 1471-2393
Titre abrégé: BMC Pregnancy Childbirth
Pays: England
ID NLM: 100967799

Informations de publication

Date de publication:
04 Oct 2024
Historique:
received: 22 06 2024
accepted: 20 09 2024
medline: 5 10 2024
pubmed: 5 10 2024
entrez: 4 10 2024
Statut: epublish

Résumé

Escherichia coli (E. coli) is one of the main bacteria associated with preterm premature rupture of membranes by increasing pro-matrix metalloproteinase 9 (proMMP-9) and degradation of type IV collagen in human feto-maternal interface (HFMi). proMMP-9 is regulated by progesterone (P4) but it is unclear whether P4 inhibits proMMP in human maternal decidual (MDec). This study aimed to determine a role of P4 on proMMP-2 and - 9 and type IV collagen induced by E. coli infection in MDec. Nine HFMi were mounted in a Transwell system. MDec was stimulated with P4 or E. coli for 3-, 6-, or 24-hours. proMMP-2, -9 and type IV collagen were assessed. Gelatin zymography revealed an increase in proMMP-9 after 3, 6, and 24 h of stimulating MDec with E. coli. Using immunofluorescence, it was confirmed the increase in the HFMi tissue and a reduction on the amount of type IV collagen leading to the separation of fetal amniochorion and MDEc. The degradative activity of proMMP-9 was reduced by 20% by coincubation with P4. P4 modulates the activity of proMMP-9 induced by E. coli stimulation but it was unable to completely reverse the degradation of type IV collagen in human MDec tissue.

Sections du résumé

BACKGROUND BACKGROUND
Escherichia coli (E. coli) is one of the main bacteria associated with preterm premature rupture of membranes by increasing pro-matrix metalloproteinase 9 (proMMP-9) and degradation of type IV collagen in human feto-maternal interface (HFMi). proMMP-9 is regulated by progesterone (P4) but it is unclear whether P4 inhibits proMMP in human maternal decidual (MDec). This study aimed to determine a role of P4 on proMMP-2 and - 9 and type IV collagen induced by E. coli infection in MDec.
METHODS METHODS
Nine HFMi were mounted in a Transwell system. MDec was stimulated with P4 or E. coli for 3-, 6-, or 24-hours. proMMP-2, -9 and type IV collagen were assessed.
RESULTS RESULTS
Gelatin zymography revealed an increase in proMMP-9 after 3, 6, and 24 h of stimulating MDec with E. coli. Using immunofluorescence, it was confirmed the increase in the HFMi tissue and a reduction on the amount of type IV collagen leading to the separation of fetal amniochorion and MDEc. The degradative activity of proMMP-9 was reduced by 20% by coincubation with P4.
CONCLUSIONS CONCLUSIONS
P4 modulates the activity of proMMP-9 induced by E. coli stimulation but it was unable to completely reverse the degradation of type IV collagen in human MDec tissue.

Identifiants

pubmed: 39367340
doi: 10.1186/s12884-024-06847-8
pii: 10.1186/s12884-024-06847-8
doi:

Substances chimiques

Progesterone 4G7DS2Q64Y
Matrix Metalloproteinase 9 EC 3.4.24.35
Collagen Type IV 0
MMP9 protein, human EC 3.4.24.35

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

645

Subventions

Organisme : Instituto Nacional de Perinatología "Isidro Espinosa de los Reyes", Ciudad de México, México.
ID : 2017-2-82

Informations de copyright

© 2024. The Author(s).

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Auteurs

Gerardo Bautista-Bautista (G)

Departamento de Inmunobioquímica, Instituto Nacional de Perinatología Isidro Espinosa de los Reyes, Urales #800 Col. Lomas de Virreyes CP 11000, Tercer piso de la Torre de Investigación, Ciudad de México, México.

Santos Salguero-Zacarias (S)

Departamento de Tococirugia y Urgencias, Instituto Nacional de Perinatología Isidro Espinosa de los Reyes, Ciudad de México, México.

Graciela Villeda-Gabriel (G)

Departamento de Inmunología e infectología, Instituto Nacional de Perinatología Isidro Espinosa de los Reyes, Ciudad de México, México.

Guadalupe García-López (G)

Departamento de Fisiología y Desarrollo Celular, Instituto Nacional de Perinatología Isidro Espinosa de los Reyes , Ciudad de México, México.

Mauricio Osorio-Caballero (M)

Departamento de Salud Sexual y Reproductiva, Instituto Nacional de Perinatología Isidro Espinosa de los Reyes, Ciudad de México, México.

Martha Leticia Palafox-Vargas (ML)

Departamento de Anatomía Patológica, Instituto Nacional de Perinatología Isidro Espinosa de los Reyes, Ciudad de México, México.

Ricardo Josué Acuña-González (RJ)

Departamento de Inmunobioquímica, Instituto Nacional de Perinatología Isidro Espinosa de los Reyes, Urales #800 Col. Lomas de Virreyes CP 11000, Tercer piso de la Torre de Investigación, Ciudad de México, México.

Irlando Lara-Pereyra (I)

Departamento de Ginecología, Hospital General de Zona 252, Instituto Mexicano del Seguro Social, Atlacomulco, México.

Oscar Díaz-Ruíz (O)

Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA.

Hector Flores-Herrera (H)

Departamento de Inmunobioquímica, Instituto Nacional de Perinatología Isidro Espinosa de los Reyes, Urales #800 Col. Lomas de Virreyes CP 11000, Tercer piso de la Torre de Investigación, Ciudad de México, México. h.flores@inper.gob.mx.

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