Melola Discovery

← Melola Discovery

Jurnal SINTA 1

Induction of Matrix Metalloproteinases in Chondrocytes by Interleukin IL-1β as an Osteoarthritis Model

Journal of Mathematical and Fundamental Sciences · Vol. 51 No. 2 (2019) · hlm. 103–111

DOI
10.5614/j.math.fund.sci.2019.51.2.1
ISSN
2338-5510, 2337-5760
Terbit
2019-08-02
Penerbit
Directorate for Research and Innovation (DRI) ITB
Bahasa
eng

Abstrak

Osteoarthritis (OA) is a chronic disease of the joints and bones due to trauma or other joint-related diseases (secondary). Synovial inflammation commonly causes disturbance in joint homeostasis, which is associated with OA. Enzymes such as aggrecanase and metalloproteinase generate cartilage damage, mediated by tumor necrosis factor (TNF-α) and interleukin (IL)-1. Pro-inflammatory cytokines, including TNF-α, IL-1β, and IL-6, are responsible for regulation of the extracellular matrix, cartilage degradation, and apoptosis of chondrocytes. This study aimed to observe the cell viability and expression level of matrix metalloproteinases (MMP-1 and MMP-3) and tissue inhibitor metalloproteinases (TIMP-1 and TIMP-2) in human chondrocyte cells (CHON-002) induced by IL-1β. CHON-002 was induced with IL-1β (0.1, 1 and 10 ng/mL) as an OA model. The viability of the cells was measured with a 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxyme-thoxyphenyl)-2-(4-sulfophenyl)-2H-tetra zolium (MTS) assay, while expression of MMP-1, MMP-3, TIMP-1, and TIMP-2, was evaluated by RT-PCR. The viability of IL-1β-induced CHON-002 (CHON-002- IL-1β) cells at day 1 and 5 showed that treatment with up to 10 ng/mL of IL-1β was not toxic. Expression of TIMP-1 and TIMP-2 in CHON-002-IL-1β was lower compared to control, while that of MMP-1 and MMP-3 was higher compared to control. These results indicate that CHON-002 treated with 10 ng/mL IL-1β has expression patterns consistent with chondrocyte damage, so the CHON-002-IL-1β system may serve as a model for MMP induction in OA.

Kata kunci

Jaringan kolaborasi para penulis

40 penulis · 203 tautan kepenulisan bersama · 82 lintas organisasi · menampilkan 40 yang paling banyak terhubung

Arahkan kursor atau ketuk sebuah nama untuk menyorot rekan penulisnya. Klik dua kali untuk membuka halaman penulis.

  • Maranatha Christian University
  • Universitas Prima Indonesia
  • National Research and Innovation Agency
  • Indonesian Institute of Sciences
  • University of Indonesia
  • Bandung Institute of Technology
  • IPB University
  • Organisasi lain
  • Afiliasi tidak diketahui
  • Organisasi berbeda
  • Organisasi sama
  • Afiliasi tidak diketahui
  • Garis lebih tebal = lebih banyak artikel bersama · lingkaran lebih besar = lebih banyak artikel
Tampilkan sebagai tabel
Rekan penulisOrganisasiArtikel bersama
Hanna Sari Widya KusumaAfiliasi tidak diketahui19
Ermi GirsangUniversitas Prima Indonesia8
Diana Krisanti JasaputraMaranatha Christian University8
Philips OnggowidjajaMaranatha Christian University8
Didik PriyandokoIndonesia University of Education7
Chrismis Novalinda GintingUniversitas Prima Indonesia6
Dhanar Septyawan HadiprasetyoUniversitas Jenderal Achmad Yani5
Hana RatnawatiMaranatha Christian University5
I Nyoman Ehrich ListerUniversitas Prima Indonesia5
Lusiana DarsonoMaranatha Christian University5
Chandra RisdianIndonesian Institute of Sciences5
Wahyu Setia WidodoAfiliasi tidak diketahui5
Rizal AzisUniversity of Indonesia4
Teresa Liliana WargasetiaMaranatha Christian University4
Ahmad FariedPadjadjaran University4
Ika Adhani SholihahBandung Institute of Technology4
Dian Ratih LaksmitawatiAfiliasi tidak diketahui4
Gian PrimahanaNational Research and Innovation Agency3
Sofa FajriahNational Research and Innovation Agency3
Ricson P. HutagaolUniversitas Nusa Bangsa3
Arief BoedionoIPB University3
Mawar SubangkitIPB University3
The Fransiska EltaniaMaranatha Christian University2
Agung NoviantoPadjadjaran University2
Muhammad Eka PrastyaNational Research and Innovation Agency2
Fadhilah Haifa ZahirohAfiliasi tidak diketahui2
Lilis Puspa FriliansariAfiliasi tidak diketahui1
Gina KhairinisaAfiliasi tidak diketahui1
Eki HerawatiAfiliasi tidak diketahui1

Afiliasi berasal dari OpenAlex; metadata OAI-PMH jurnal tidak memuatnya. Penulis tanpa ID OpenAlex dicocokkan berdasarkan nama, sehingga dua orang bisa tergabung atau satu orang bisa terpisah.

Sumber metadata: OAI-PMH (metadata jurnal) https://journals.itb.ac.id/index.php/jmfs/oai, pertama di-harvest 9 Nov 2026, terakhir terlihat 9 Nov 2026.
Metadata asli (oai_dc)
<oai_dc:dc xmlns="http://www.openarchives.org/OAI/2.0/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/  http://www.openarchives.org/OAI/2.0/oai_dc.xsd">
	<dc:title xml:lang="en-US">Induction of Matrix Metalloproteinases in Chondrocytes by Interleukin IL-1β as an Osteoarthritis Model</dc:title>
	<dc:creator>Afifah, Ervi</dc:creator>
	<dc:creator>Mozef, Tjandrawati</dc:creator>
	<dc:creator>Sandra, Ferry</dc:creator>
	<dc:creator>Arumwardana, Seila</dc:creator>
	<dc:creator>Rihibiha, Dwi Davidson</dc:creator>
	<dc:creator>Nufus, Hayatun</dc:creator>
	<dc:creator>Rizal, Rizal</dc:creator>
	<dc:creator>Amalia, Annisa</dc:creator>
	<dc:creator>Bachtiar, Indra</dc:creator>
	<dc:creator>Murti, Harry</dc:creator>
	<dc:creator>Widowati, Wahyu</dc:creator>
	<dc:subject xml:lang="en-US">interleukin</dc:subject>
	<dc:subject xml:lang="en-US">mesenchymal stem cell</dc:subject>
	<dc:subject xml:lang="en-US">metalloproteases</dc:subject>
	<dc:subject xml:lang="en-US">MMP genes</dc:subject>
	<dc:subject xml:lang="en-US">osteoarthritis</dc:subject>
	<dc:description xml:lang="en-US">Osteoarthritis (OA) is a chronic disease of the joints and bones due to trauma or other joint-related diseases (secondary). Synovial inflammation commonly causes disturbance in joint homeostasis, which is associated with OA. Enzymes such as aggrecanase and metalloproteinase generate cartilage damage, mediated by tumor necrosis factor (TNF-α) and interleukin (IL)-1. Pro-inflammatory cytokines, including TNF-α, IL-1β, and IL-6, are responsible for regulation of the extracellular matrix, cartilage degradation, and apoptosis of chondrocytes. This study aimed to observe the cell viability and expression level of matrix metalloproteinases (MMP-1 and MMP-3) and tissue inhibitor metalloproteinases (TIMP-1 and TIMP-2) in human chondrocyte cells (CHON-002) induced by IL-1β. CHON-002 was induced with IL-1β (0.1, 1 and 10 ng/mL) as an OA model. The viability of the cells was measured with a 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxyme-thoxyphenyl)-2-(4-sulfophenyl)-2H-tetra zolium (MTS) assay, while expression of MMP-1, MMP-3, TIMP-1, and TIMP-2, was evaluated by RT-PCR. The viability of IL-1β-induced CHON-002 (CHON-002- IL-1β) cells at day 1 and 5 showed that treatment with up to 10 ng/mL of IL-1β was not toxic. Expression of TIMP-1 and TIMP-2 in CHON-002-IL-1β was lower compared to control, while that of MMP-1 and MMP-3 was higher compared to control. These results indicate that CHON-002 treated with 10 ng/mL IL-1β has expression patterns consistent with chondrocyte damage, so the CHON-002-IL-1β system may serve as a model for MMP induction in OA.</dc:description>
	<dc:publisher xml:lang="en-US">Directorate for Research and Innovation (DRI) ITB</dc:publisher>
	<dc:date>2019-08-02</dc:date>
	<dc:type>info:eu-repo/semantics/article</dc:type>
	<dc:type>info:eu-repo/semantics/publishedVersion</dc:type>
	<dc:format>application/pdf</dc:format>
	<dc:identifier>https://journals.itb.ac.id/index.php/jmfs/article/view/8428</dc:identifier>
	<dc:identifier>10.5614/j.math.fund.sci.2019.51.2.1</dc:identifier>
	<dc:source xml:lang="en-US">Journal of Mathematical and Fundamental Sciences; Vol. 51 No. 2 (2019); 103-111</dc:source>
	<dc:source>2338-5510</dc:source>
	<dc:source>2337-5760</dc:source>
	<dc:source>10.5614/j.math.fund.sci.2019.51.2</dc:source>
	<dc:language>eng</dc:language>
	<dc:relation>https://journals.itb.ac.id/index.php/jmfs/article/view/8428/3837</dc:relation>
</oai_dc:dc>