Surface roughness mediates its effects on osteoblasts via protein kinase A and phospholipase A2

Barbara D. Boyan, Victor L. Sylvia, Yuhong Liu, Ruben Sagun, David L Cochran, Christoph H. Lohmann, David D Dean, Zvi Schwartz

Research output: Contribution to journalArticle

108 Citations (Scopus)

Abstract

Earlier studies have shown that implant surface roughness influences osteoblast proliferation, differentiation, matrix synthesis and local factor production. Moreover, the responsiveness of osteoblasts to systemic hormones, such as 1,25-(OH)2D3, at the implant surface is also influenced by surface roughness and this effect is mediated by changes in prostaglandins. At present, it is not known which signaling pathways are involved in mediating cell response to surface roughness and how 1,25-(OH)2D3 treatment alters the activation of these pathways. This paper reviews a series of studies that have addressed this question. MG63 osteoblast-like cells were cultured on commercially pure titanium (cpTi) surfaces of two different roughnesses (R(a) 0.54 and 4.92μm) in the presence of control media or media containing 1,25-(OH)2D3 or 1,25-(OH)2D3 plus H8 (a protein kinase A inhibitor) or quinacrine (a phospholipase A2 inhibitor). At harvest, the effect of these treatments on cell number and alkaline phosphatase specific activity was measured. Compared to cultures grown on the smooth surface, cell number was reduced on the rough surface. 1,25-(OH)2D3 inhibited cell number on both surfaces and inhibition of protein kinase A in the presence of 1,25-(OH)2D3 restored cell number to that seen in the control cultures. Inhibition of phospholipase A2 in the presence of 1,25-(OH)2D3 caused a further reduction in cell number on the smooth surface, and partially reversed the inhibitory effects of 1,25-(OH)2D3 on the rough surface. Alkaline phosphatase specific activity was increased in cultures grown on the rough surface compared with those grown on the smooth surface; 1,25-(OH)2D3 treatment increased enzyme specific activity on both surfaces. Cultures treated with H8 and 1,25-(OH)2D3 displayed enzyme specific activity that approximated that seen in control cultures. Inhibition of phospholipase A2 also inhibited the 1,25-(OH)2D3-dependent effect on the smooth surface, but on the rough surface there was an inhibition of the 1,25-(OH)2D3 effect as well as a partial inhibition of the surface roughness-dependent effect. The results indicate that surface roughness and 1,25-(OH)2D3 mediate their effects through phospholipase A2, which catalyzes one of the rate-limiting steps in prostaglandin E2 production. Further downstream, prostaglandin E2 activates protein kinase A. Copyright (C) 1999 Elsevier Science Ltd.

Original languageEnglish (US)
Pages (from-to)2305-2310
Number of pages6
JournalBiomaterials
Volume20
Issue number23-24
DOIs
StatePublished - Dec 1999

Fingerprint

Phospholipases A2
Osteoblasts
Cyclic AMP-Dependent Protein Kinases
Cell Count
Surface roughness
Proteins
Dinoprostone
Alkaline Phosphatase
Quinacrine
Enzymes
Protein Kinase Inhibitors
Titanium
Phosphatases
Prostaglandins
Cultured Cells
Membrane Proteins
Hormones
Chemical activation

Keywords

  • 1,25-(OH)D
  • MG63 cells
  • Osteoblasts
  • Phospholipase A
  • PKA
  • PLA
  • Protein kinase A
  • Surface roughness
  • Titanium

ASJC Scopus subject areas

  • Biotechnology
  • Bioengineering
  • Biomedical Engineering

Cite this

Boyan, B. D., Sylvia, V. L., Liu, Y., Sagun, R., Cochran, D. L., H. Lohmann, C., ... Schwartz, Z. (1999). Surface roughness mediates its effects on osteoblasts via protein kinase A and phospholipase A2 Biomaterials, 20(23-24), 2305-2310. https://doi.org/10.1016/S0142-9612(99)00159-3

Surface roughness mediates its effects on osteoblasts via protein kinase A and phospholipase A2 . / Boyan, Barbara D.; Sylvia, Victor L.; Liu, Yuhong; Sagun, Ruben; Cochran, David L; H. Lohmann, Christoph; Dean, David D; Schwartz, Zvi.

In: Biomaterials, Vol. 20, No. 23-24, 12.1999, p. 2305-2310.

Research output: Contribution to journalArticle

Boyan, BD, Sylvia, VL, Liu, Y, Sagun, R, Cochran, DL, H. Lohmann, C, Dean, DD & Schwartz, Z 1999, 'Surface roughness mediates its effects on osteoblasts via protein kinase A and phospholipase A2 ', Biomaterials, vol. 20, no. 23-24, pp. 2305-2310. https://doi.org/10.1016/S0142-9612(99)00159-3
Boyan, Barbara D. ; Sylvia, Victor L. ; Liu, Yuhong ; Sagun, Ruben ; Cochran, David L ; H. Lohmann, Christoph ; Dean, David D ; Schwartz, Zvi. / Surface roughness mediates its effects on osteoblasts via protein kinase A and phospholipase A2 In: Biomaterials. 1999 ; Vol. 20, No. 23-24. pp. 2305-2310.
@article{7702d4d92ebc47d581a8ca3a31820cdb,
title = "Surface roughness mediates its effects on osteoblasts via protein kinase A and phospholipase A2",
abstract = "Earlier studies have shown that implant surface roughness influences osteoblast proliferation, differentiation, matrix synthesis and local factor production. Moreover, the responsiveness of osteoblasts to systemic hormones, such as 1,25-(OH)2D3, at the implant surface is also influenced by surface roughness and this effect is mediated by changes in prostaglandins. At present, it is not known which signaling pathways are involved in mediating cell response to surface roughness and how 1,25-(OH)2D3 treatment alters the activation of these pathways. This paper reviews a series of studies that have addressed this question. MG63 osteoblast-like cells were cultured on commercially pure titanium (cpTi) surfaces of two different roughnesses (R(a) 0.54 and 4.92μm) in the presence of control media or media containing 1,25-(OH)2D3 or 1,25-(OH)2D3 plus H8 (a protein kinase A inhibitor) or quinacrine (a phospholipase A2 inhibitor). At harvest, the effect of these treatments on cell number and alkaline phosphatase specific activity was measured. Compared to cultures grown on the smooth surface, cell number was reduced on the rough surface. 1,25-(OH)2D3 inhibited cell number on both surfaces and inhibition of protein kinase A in the presence of 1,25-(OH)2D3 restored cell number to that seen in the control cultures. Inhibition of phospholipase A2 in the presence of 1,25-(OH)2D3 caused a further reduction in cell number on the smooth surface, and partially reversed the inhibitory effects of 1,25-(OH)2D3 on the rough surface. Alkaline phosphatase specific activity was increased in cultures grown on the rough surface compared with those grown on the smooth surface; 1,25-(OH)2D3 treatment increased enzyme specific activity on both surfaces. Cultures treated with H8 and 1,25-(OH)2D3 displayed enzyme specific activity that approximated that seen in control cultures. Inhibition of phospholipase A2 also inhibited the 1,25-(OH)2D3-dependent effect on the smooth surface, but on the rough surface there was an inhibition of the 1,25-(OH)2D3 effect as well as a partial inhibition of the surface roughness-dependent effect. The results indicate that surface roughness and 1,25-(OH)2D3 mediate their effects through phospholipase A2, which catalyzes one of the rate-limiting steps in prostaglandin E2 production. Further downstream, prostaglandin E2 activates protein kinase A. Copyright (C) 1999 Elsevier Science Ltd.",
keywords = "1,25-(OH)D, MG63 cells, Osteoblasts, Phospholipase A, PKA, PLA, Protein kinase A, Surface roughness, Titanium",
author = "Boyan, {Barbara D.} and Sylvia, {Victor L.} and Yuhong Liu and Ruben Sagun and Cochran, {David L} and {H. Lohmann}, Christoph and Dean, {David D} and Zvi Schwartz",
year = "1999",
month = "12",
doi = "10.1016/S0142-9612(99)00159-3",
language = "English (US)",
volume = "20",
pages = "2305--2310",
journal = "Biomaterials",
issn = "0142-9612",
publisher = "Elsevier BV",
number = "23-24",

}

TY - JOUR

T1 - Surface roughness mediates its effects on osteoblasts via protein kinase A and phospholipase A2

AU - Boyan, Barbara D.

AU - Sylvia, Victor L.

AU - Liu, Yuhong

AU - Sagun, Ruben

AU - Cochran, David L

AU - H. Lohmann, Christoph

AU - Dean, David D

AU - Schwartz, Zvi

PY - 1999/12

Y1 - 1999/12

N2 - Earlier studies have shown that implant surface roughness influences osteoblast proliferation, differentiation, matrix synthesis and local factor production. Moreover, the responsiveness of osteoblasts to systemic hormones, such as 1,25-(OH)2D3, at the implant surface is also influenced by surface roughness and this effect is mediated by changes in prostaglandins. At present, it is not known which signaling pathways are involved in mediating cell response to surface roughness and how 1,25-(OH)2D3 treatment alters the activation of these pathways. This paper reviews a series of studies that have addressed this question. MG63 osteoblast-like cells were cultured on commercially pure titanium (cpTi) surfaces of two different roughnesses (R(a) 0.54 and 4.92μm) in the presence of control media or media containing 1,25-(OH)2D3 or 1,25-(OH)2D3 plus H8 (a protein kinase A inhibitor) or quinacrine (a phospholipase A2 inhibitor). At harvest, the effect of these treatments on cell number and alkaline phosphatase specific activity was measured. Compared to cultures grown on the smooth surface, cell number was reduced on the rough surface. 1,25-(OH)2D3 inhibited cell number on both surfaces and inhibition of protein kinase A in the presence of 1,25-(OH)2D3 restored cell number to that seen in the control cultures. Inhibition of phospholipase A2 in the presence of 1,25-(OH)2D3 caused a further reduction in cell number on the smooth surface, and partially reversed the inhibitory effects of 1,25-(OH)2D3 on the rough surface. Alkaline phosphatase specific activity was increased in cultures grown on the rough surface compared with those grown on the smooth surface; 1,25-(OH)2D3 treatment increased enzyme specific activity on both surfaces. Cultures treated with H8 and 1,25-(OH)2D3 displayed enzyme specific activity that approximated that seen in control cultures. Inhibition of phospholipase A2 also inhibited the 1,25-(OH)2D3-dependent effect on the smooth surface, but on the rough surface there was an inhibition of the 1,25-(OH)2D3 effect as well as a partial inhibition of the surface roughness-dependent effect. The results indicate that surface roughness and 1,25-(OH)2D3 mediate their effects through phospholipase A2, which catalyzes one of the rate-limiting steps in prostaglandin E2 production. Further downstream, prostaglandin E2 activates protein kinase A. Copyright (C) 1999 Elsevier Science Ltd.

AB - Earlier studies have shown that implant surface roughness influences osteoblast proliferation, differentiation, matrix synthesis and local factor production. Moreover, the responsiveness of osteoblasts to systemic hormones, such as 1,25-(OH)2D3, at the implant surface is also influenced by surface roughness and this effect is mediated by changes in prostaglandins. At present, it is not known which signaling pathways are involved in mediating cell response to surface roughness and how 1,25-(OH)2D3 treatment alters the activation of these pathways. This paper reviews a series of studies that have addressed this question. MG63 osteoblast-like cells were cultured on commercially pure titanium (cpTi) surfaces of two different roughnesses (R(a) 0.54 and 4.92μm) in the presence of control media or media containing 1,25-(OH)2D3 or 1,25-(OH)2D3 plus H8 (a protein kinase A inhibitor) or quinacrine (a phospholipase A2 inhibitor). At harvest, the effect of these treatments on cell number and alkaline phosphatase specific activity was measured. Compared to cultures grown on the smooth surface, cell number was reduced on the rough surface. 1,25-(OH)2D3 inhibited cell number on both surfaces and inhibition of protein kinase A in the presence of 1,25-(OH)2D3 restored cell number to that seen in the control cultures. Inhibition of phospholipase A2 in the presence of 1,25-(OH)2D3 caused a further reduction in cell number on the smooth surface, and partially reversed the inhibitory effects of 1,25-(OH)2D3 on the rough surface. Alkaline phosphatase specific activity was increased in cultures grown on the rough surface compared with those grown on the smooth surface; 1,25-(OH)2D3 treatment increased enzyme specific activity on both surfaces. Cultures treated with H8 and 1,25-(OH)2D3 displayed enzyme specific activity that approximated that seen in control cultures. Inhibition of phospholipase A2 also inhibited the 1,25-(OH)2D3-dependent effect on the smooth surface, but on the rough surface there was an inhibition of the 1,25-(OH)2D3 effect as well as a partial inhibition of the surface roughness-dependent effect. The results indicate that surface roughness and 1,25-(OH)2D3 mediate their effects through phospholipase A2, which catalyzes one of the rate-limiting steps in prostaglandin E2 production. Further downstream, prostaglandin E2 activates protein kinase A. Copyright (C) 1999 Elsevier Science Ltd.

KW - 1,25-(OH)D

KW - MG63 cells

KW - Osteoblasts

KW - Phospholipase A

KW - PKA

KW - PLA

KW - Protein kinase A

KW - Surface roughness

KW - Titanium

UR - http://www.scopus.com/inward/record.url?scp=0032730247&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0032730247&partnerID=8YFLogxK

U2 - 10.1016/S0142-9612(99)00159-3

DO - 10.1016/S0142-9612(99)00159-3

M3 - Article

C2 - 10614936

AN - SCOPUS:0032730247

VL - 20

SP - 2305

EP - 2310

JO - Biomaterials

JF - Biomaterials

SN - 0142-9612

IS - 23-24

ER -