Surface expression of fatty acid translocase [FAT/CD36] on platelets in myeloproliferative disease and non-insulin dependent diabetes mellitus: effect on arachidonic acid uptake

H. Salah-Uddin, M. J. Gordon, Isobel Ford, N. N. Tandon, Michael Greaves, A. K. Dutta Roy

Research output: Contribution to journalArticle

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Abstract

Increased platelet reactivity has been implicated in the vascular complications of myeloproliferative diseases and diabetes mellitus. The mechanisms of platelet hyperresponsiveness have not been fully explained. Expression of CD36 or fatty acid translocase (FAT) and its role in arachidonic acid (AA) uptake by platelets were examined in subjects with myeloproliferative disorders (MPD), those with non-insulin-dependent diabetes mellitus (NIDDM), and in normal, healthy, age-matched controls. Surface expression of CD36 on platelet membranes was increased in MPD (10.94 +/- 0.76 pmol/mg protein) compared with normal controls (6.94 +/- 0.48 pmol/mg protein), p < 0.001. Total platelet content of CD36 was also significantly higher (32.1 &PLUSMN; 0.61 pmol/mg protein, p < 0.01) compared with those in sex and age matched normal controls (25.7 +/- 1.09 pmol/mg protein). In contrast, platelet surface expression of CD36 in NIDDM (6.5 +/- 0.56 pmol/mg protein) was not significantly different from those of normal controls despite higher total content of CD36 (32.8 +/- 1.2,, pmol/mg protein, p < 0.01). Intact MPD platelets bound significantly more arachidonic acid (AA) (1.53 &PLUSMN; 0.16 nmol/mg protein, p < 0.05), compared with controls (1.12 +/- 0.07 nmol/mg protein) or NIDDM subjects (1.16 +/- 0.16 nmol/mg protein). The capacity of MPD platelet membranes to bind C-14-AA was also increased (1.72 +/- 0.25 nmol/mg protein, p < 0.05) compared with that of controls (1.62 &PLUSMN; 0.05 nmol/mg protein) and of NIDDM (1.22 &PLUSMN; 0.08 nmol/mg protein). This is consistent with higher surface expression of CD36 in MPD platelets. Membrane fatty acid analysis indicated that the % of AA in platelet phospholipids was significantly lower in MPD (3.15 &PLUSMN; 0.81%) compared with the controls (5.62 &PLUSMN; 1.7%, p < 0.05. The AA content of diabetic platelets (4.82 +/- 1.1%) was not significantly different from normal controls. In summary, both total and surface expression of CD36 are increased in MPD, consistent with an enhanced capacity for uptake of AA by platelets. Increased expression of CD36 in platelets may play a role in the vaso-occlusive manifestations of MPD.

Original languageEnglish
Pages (from-to)203-211
Number of pages8
JournalMolecular & Cellular Biochemistry
Volume239
DOIs
Publication statusPublished - 2002

Keywords

  • FAT
  • CD36
  • fatty acid translocase
  • arachidonic acid
  • platelets
  • diabetes
  • myeloproliferative disorders
  • fatty acid uptake
  • thromboxane A2
  • membrane phospholipids
  • LOW-DENSITY-LIPOPROTEIN
  • GLYCOPROTEIN-IIB-IIIA
  • HUMAN PLACENTA
  • POLYCYTHEMIA-VERA
  • BINDING PROTEIN
  • IV CD36
  • ACTIVATION
  • ADHESION
  • PLASMA
  • BLOOD

Cite this

Surface expression of fatty acid translocase [FAT/CD36] on platelets in myeloproliferative disease and non-insulin dependent diabetes mellitus: effect on arachidonic acid uptake. / Salah-Uddin, H.; Gordon, M. J.; Ford, Isobel; Tandon, N. N.; Greaves, Michael; Dutta Roy, A. K.

In: Molecular & Cellular Biochemistry, Vol. 239, 2002, p. 203-211.

Research output: Contribution to journalArticle

Salah-Uddin, H. ; Gordon, M. J. ; Ford, Isobel ; Tandon, N. N. ; Greaves, Michael ; Dutta Roy, A. K. / Surface expression of fatty acid translocase [FAT/CD36] on platelets in myeloproliferative disease and non-insulin dependent diabetes mellitus: effect on arachidonic acid uptake. In: Molecular & Cellular Biochemistry. 2002 ; Vol. 239. pp. 203-211.
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abstract = "Increased platelet reactivity has been implicated in the vascular complications of myeloproliferative diseases and diabetes mellitus. The mechanisms of platelet hyperresponsiveness have not been fully explained. Expression of CD36 or fatty acid translocase (FAT) and its role in arachidonic acid (AA) uptake by platelets were examined in subjects with myeloproliferative disorders (MPD), those with non-insulin-dependent diabetes mellitus (NIDDM), and in normal, healthy, age-matched controls. Surface expression of CD36 on platelet membranes was increased in MPD (10.94 +/- 0.76 pmol/mg protein) compared with normal controls (6.94 +/- 0.48 pmol/mg protein), p < 0.001. Total platelet content of CD36 was also significantly higher (32.1 &PLUSMN; 0.61 pmol/mg protein, p < 0.01) compared with those in sex and age matched normal controls (25.7 +/- 1.09 pmol/mg protein). In contrast, platelet surface expression of CD36 in NIDDM (6.5 +/- 0.56 pmol/mg protein) was not significantly different from those of normal controls despite higher total content of CD36 (32.8 +/- 1.2,, pmol/mg protein, p < 0.01). Intact MPD platelets bound significantly more arachidonic acid (AA) (1.53 &PLUSMN; 0.16 nmol/mg protein, p < 0.05), compared with controls (1.12 +/- 0.07 nmol/mg protein) or NIDDM subjects (1.16 +/- 0.16 nmol/mg protein). The capacity of MPD platelet membranes to bind C-14-AA was also increased (1.72 +/- 0.25 nmol/mg protein, p < 0.05) compared with that of controls (1.62 &PLUSMN; 0.05 nmol/mg protein) and of NIDDM (1.22 &PLUSMN; 0.08 nmol/mg protein). This is consistent with higher surface expression of CD36 in MPD platelets. Membrane fatty acid analysis indicated that the {\%} of AA in platelet phospholipids was significantly lower in MPD (3.15 &PLUSMN; 0.81{\%}) compared with the controls (5.62 &PLUSMN; 1.7{\%}, p < 0.05. The AA content of diabetic platelets (4.82 +/- 1.1{\%}) was not significantly different from normal controls. In summary, both total and surface expression of CD36 are increased in MPD, consistent with an enhanced capacity for uptake of AA by platelets. Increased expression of CD36 in platelets may play a role in the vaso-occlusive manifestations of MPD.",
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T1 - Surface expression of fatty acid translocase [FAT/CD36] on platelets in myeloproliferative disease and non-insulin dependent diabetes mellitus: effect on arachidonic acid uptake

AU - Salah-Uddin, H.

AU - Gordon, M. J.

AU - Ford, Isobel

AU - Tandon, N. N.

AU - Greaves, Michael

AU - Dutta Roy, A. K.

PY - 2002

Y1 - 2002

N2 - Increased platelet reactivity has been implicated in the vascular complications of myeloproliferative diseases and diabetes mellitus. The mechanisms of platelet hyperresponsiveness have not been fully explained. Expression of CD36 or fatty acid translocase (FAT) and its role in arachidonic acid (AA) uptake by platelets were examined in subjects with myeloproliferative disorders (MPD), those with non-insulin-dependent diabetes mellitus (NIDDM), and in normal, healthy, age-matched controls. Surface expression of CD36 on platelet membranes was increased in MPD (10.94 +/- 0.76 pmol/mg protein) compared with normal controls (6.94 +/- 0.48 pmol/mg protein), p < 0.001. Total platelet content of CD36 was also significantly higher (32.1 &PLUSMN; 0.61 pmol/mg protein, p < 0.01) compared with those in sex and age matched normal controls (25.7 +/- 1.09 pmol/mg protein). In contrast, platelet surface expression of CD36 in NIDDM (6.5 +/- 0.56 pmol/mg protein) was not significantly different from those of normal controls despite higher total content of CD36 (32.8 +/- 1.2,, pmol/mg protein, p < 0.01). Intact MPD platelets bound significantly more arachidonic acid (AA) (1.53 &PLUSMN; 0.16 nmol/mg protein, p < 0.05), compared with controls (1.12 +/- 0.07 nmol/mg protein) or NIDDM subjects (1.16 +/- 0.16 nmol/mg protein). The capacity of MPD platelet membranes to bind C-14-AA was also increased (1.72 +/- 0.25 nmol/mg protein, p < 0.05) compared with that of controls (1.62 &PLUSMN; 0.05 nmol/mg protein) and of NIDDM (1.22 &PLUSMN; 0.08 nmol/mg protein). This is consistent with higher surface expression of CD36 in MPD platelets. Membrane fatty acid analysis indicated that the % of AA in platelet phospholipids was significantly lower in MPD (3.15 &PLUSMN; 0.81%) compared with the controls (5.62 &PLUSMN; 1.7%, p < 0.05. The AA content of diabetic platelets (4.82 +/- 1.1%) was not significantly different from normal controls. In summary, both total and surface expression of CD36 are increased in MPD, consistent with an enhanced capacity for uptake of AA by platelets. Increased expression of CD36 in platelets may play a role in the vaso-occlusive manifestations of MPD.

AB - Increased platelet reactivity has been implicated in the vascular complications of myeloproliferative diseases and diabetes mellitus. The mechanisms of platelet hyperresponsiveness have not been fully explained. Expression of CD36 or fatty acid translocase (FAT) and its role in arachidonic acid (AA) uptake by platelets were examined in subjects with myeloproliferative disorders (MPD), those with non-insulin-dependent diabetes mellitus (NIDDM), and in normal, healthy, age-matched controls. Surface expression of CD36 on platelet membranes was increased in MPD (10.94 +/- 0.76 pmol/mg protein) compared with normal controls (6.94 +/- 0.48 pmol/mg protein), p < 0.001. Total platelet content of CD36 was also significantly higher (32.1 &PLUSMN; 0.61 pmol/mg protein, p < 0.01) compared with those in sex and age matched normal controls (25.7 +/- 1.09 pmol/mg protein). In contrast, platelet surface expression of CD36 in NIDDM (6.5 +/- 0.56 pmol/mg protein) was not significantly different from those of normal controls despite higher total content of CD36 (32.8 +/- 1.2,, pmol/mg protein, p < 0.01). Intact MPD platelets bound significantly more arachidonic acid (AA) (1.53 &PLUSMN; 0.16 nmol/mg protein, p < 0.05), compared with controls (1.12 +/- 0.07 nmol/mg protein) or NIDDM subjects (1.16 +/- 0.16 nmol/mg protein). The capacity of MPD platelet membranes to bind C-14-AA was also increased (1.72 +/- 0.25 nmol/mg protein, p < 0.05) compared with that of controls (1.62 &PLUSMN; 0.05 nmol/mg protein) and of NIDDM (1.22 &PLUSMN; 0.08 nmol/mg protein). This is consistent with higher surface expression of CD36 in MPD platelets. Membrane fatty acid analysis indicated that the % of AA in platelet phospholipids was significantly lower in MPD (3.15 &PLUSMN; 0.81%) compared with the controls (5.62 &PLUSMN; 1.7%, p < 0.05. The AA content of diabetic platelets (4.82 +/- 1.1%) was not significantly different from normal controls. In summary, both total and surface expression of CD36 are increased in MPD, consistent with an enhanced capacity for uptake of AA by platelets. Increased expression of CD36 in platelets may play a role in the vaso-occlusive manifestations of MPD.

KW - FAT

KW - CD36

KW - fatty acid translocase

KW - arachidonic acid

KW - platelets

KW - diabetes

KW - myeloproliferative disorders

KW - fatty acid uptake

KW - thromboxane A2

KW - membrane phospholipids

KW - LOW-DENSITY-LIPOPROTEIN

KW - GLYCOPROTEIN-IIB-IIIA

KW - HUMAN PLACENTA

KW - POLYCYTHEMIA-VERA

KW - BINDING PROTEIN

KW - IV CD36

KW - ACTIVATION

KW - ADHESION

KW - PLASMA

KW - BLOOD

U2 - 10.1023/A:1020583630536

DO - 10.1023/A:1020583630536

M3 - Article

VL - 239

SP - 203

EP - 211

JO - Molecular & Cellular Biochemistry

JF - Molecular & Cellular Biochemistry

SN - 0300-8177

ER -