PMID- 36180273
OWN - NLM
STAT- MEDLINE
DCOM- 20221004
LR  - 20231001
IS  - 1559-4106 (Electronic)
IS  - 1934-8630 (Print)
IS  - 1559-4106 (Linking)
VI  - 17
IP  - 5
DP  - 2022 Sep 30
TI  - Interleukin 1beta and lipopolysaccharides induction dictate chondrocyte 
      morphological properties and reduce cellular roughness and adhesion energy 
      comparatively.
PG  - 051001
LID - 10.1116/6.0001986 [doi]
LID - 051001
AB  - Osteoarthritis (OA) is a whole joint disease marked by the degradation of the 
      articular cartilage (AC) tissue, chronic inflammation, and bone remodeling. Upon 
      AC's injury, proinflammatory mediators including interleukin 1beta (IL1beta) and 
      lipopolysaccharides (LPS) play major roles in the onset and progression of OA. 
      The objective of this study was to mechanistically detect and compare the effects 
      of IL1beta and LPS, separately, on the morphological and nanomechanical properties 
      of bovine chondrocytes. Cells were seeded overnight in a full serum medium and 
      the next day divided into three main groups: A negative control (NC) of a reduced 
      serum medium and 10 ng/ml IL1ss or 10 ng/ml LPS-modified media. Cells were induced 
      for 24 h. Nanomechanical properties (elastic modulus and adhesion energy) and 
      roughness were quantified using atomic force microscopy. Nitric oxide, 
      prostaglandin 2 (PGE2), and matrix metalloproteinases 3 (MMP3) contents; 
      viability of cells; and extracellular matrix components were quantified. Our data 
      revealed that viability of the cells was not affected by inflammatory induction 
      and IL1ss induction increased PGE2. Elastic moduli of cells were similar among 
      IL1beta and NC while LPS significantly decreased the elasticity compared to NC. IL1ss 
      induction resulted in least cellular roughness while LPS induction resulted in 
      least adhesion energy compared to NC. Our images suggest that IL1ss and LPS 
      inflammation affect cellular morphology with cytoskeleton rearrangements and the 
      presence of stress fibers. Finally, our results suggest that the two investigated 
      inflammatory mediators modulated chondrocytes' immediate responses to 
      inflammation in variable ways.
FAU - Mallah, Alia H
AU  - Mallah AH
AUID- ORCID: 0000-0001-9555-5583
AD  - Department of Biomedical Engineering and Chemical Engineering, The University of 
      Texas at San Antonio (UTSA), San Antonio, Texas 78249.
FAU - Amr, Mahmoud
AU  - Amr M
AUID- ORCID: 0000-0002-8555-8497
AD  - Department of Biomedical Engineering and Chemical Engineering, The University of 
      Texas at San Antonio (UTSA), San Antonio, Texas 78249.
FAU - Gozen, Arda
AU  - Gozen A
AUID- ORCID: 0000-0002-2680-2269
AD  - School of Mechanical and Materials Engineering, Washington State University, 
      Pullman, Washington 99164.
FAU - Mendenhall, Juana
AU  - Mendenhall J
AD  - Department of Chemistry, Morehouse College, Atlanta, Georgia 30314.
FAU - Van-Wie, Bernard J
AU  - Van-Wie BJ
AUID- ORCID: 0000-0001-7382-9715
AD  - Gene and Linda Voiland School of Chemical Engineering and Bioengineering, 
      Washington State University, Pullman, Washington 99164.
FAU - Abu-Lail, Nehal I
AU  - Abu-Lail NI
AUID- ORCID: 0000-0002-2319-2450
AD  - Department of Biomedical Engineering and Chemical Engineering, The University of 
      Texas at San Antonio (UTSA), San Antonio, Texas 78249.
LA  - eng
GR  - T32 GM008336/GM/NIGMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
DEP - 20220930
PL  - United States
TA  - Biointerphases
JT  - Biointerphases
JID - 101275679
RN  - 0 (Interleukin-1beta)
RN  - 0 (Lipopolysaccharides)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - EC 3.4.24.17 (Matrix Metalloproteinase 3)
RN  - K7Q1JQR04M (Dinoprostone)
SB  - IM
MH  - Animals
MH  - Cattle
MH  - Cells, Cultured
MH  - *Chondrocytes/metabolism
MH  - Dinoprostone/metabolism/pharmacology
MH  - Inflammation
MH  - Interleukin-1beta/metabolism/pharmacology
MH  - Lipopolysaccharides/toxicity
MH  - Matrix Metalloproteinase 3/metabolism/pharmacology
MH  - Nitric Oxide/pharmacology
MH  - *Osteoarthritis/metabolism
PMC - PMC9526521
EDAT- 2022/10/01 06:00
MHDA- 2022/10/05 06:00
PMCR- 2023/09/30
CRDT- 2022/09/30 22:03
PHST- 2022/09/30 22:03 [entrez]
PHST- 2022/10/01 06:00 [pubmed]
PHST- 2022/10/05 06:00 [medline]
PHST- 2023/09/30 00:00 [pmc-release]
AID - 6.0001986 [pii]
AID - 10.1116/6.0001986 [doi]
PST - epublish
SO  - Biointerphases. 2022 Sep 30;17(5):051001. doi: 10.1116/6.0001986.