Mepacrine-Labeled Platelet Dense-Body Number in Patients with Chronic Uremia

Nephron ◽  
1988 ◽  
Vol 50 (4) ◽  
pp. 306-307
Author(s):  
M. Komarnicki ◽  
I. Pietrzak ◽  
M. Zozulińska
Keyword(s):  
Dense Body ◽  
Chronic Uremia

Relationship Between Mepacrine-Labelled Dense Body Number, Platelet Capacity to Accumulate 14C-5-HT and Platelet Density in the Bernard-Soulier and Hermansky-Pudlak Syndromes

1979 ◽  
Vol 42 (02) ◽  
pp. 694-704 ◽  
Author(s):  
F Rendu ◽  
A T Nurden ◽  
M Lebret ◽  
J P Caen
Keyword(s):  
Dense Body ◽  
Human Subjects ◽  
Human Platelets ◽  
Dense Bodies ◽  
Storage Organelle ◽  
Hereditary Disorders ◽  
Labelling Procedure ◽  
Normal Human ◽  
Hermansky Pudlak Syndrome ◽  
Bernard Soulier Syndrome

SummaryWe have used the mepacrine-labelling procedure to measure the dense body (serotonin storage organelle) content of the platelets of 2 hereditary disorders where abnormalities in dense body number were suspected. The platelets were incubated with mepacrine and examined by fluorescence microscopy. A mean number of 5.4 ± 0.8 (SD) dense bodies per platelet was calculated from the data obtained using platelets isolated from 40 normal human subjects. In contrast the platelets of 2 patients with the Bernard-Soulier syndrome contained an average of 14 and 17 labelled granules. This increase was associated with a much greater capacity of the platelets to accumulate 14C-5-HT. The opposite result was obtained using the platelets from 2 patients with the Hermansky-Pudlak syndrome which contained few granules labelled by mepacrine and took up less 14C-5-HT than normal human platelets. Centrifugation of the patients’ platelets on discontinuous sucrose gradients showed that the platelets of the 2 Bemard-Soulier patients were much denser than normal whereas a high proportion of low density platelets was observed in the Hermansky-Pudlak syndrome. These results further define the platelet abnormalities in the two syndromes and suggest that dense body number may be one of the factors governing platelet density.

scholarly journals The basal component of the nematode dense-body is vinculin

1989 ◽  
Vol 264 (17) ◽  
pp. 10177-10185
Author(s):  
R J Barstead ◽  
R H Waterston
Keyword(s):  
Dense Body

A New Type of Artificial Kidney. II. Treatment of Acute and Chronic Uremia

1953 ◽  
Vol 69 (6) ◽  
pp. 753-759 ◽  
Author(s):  
George Hollander ◽  
Julian A. Sterling ◽  
Joseph C. Doane
Keyword(s):  
Artificial Kidney ◽  
Chronic Uremia ◽  
New Type

scholarly journals AP-3 Mediates Tyrosinase but Not TRP-1 Trafficking in Human Melanocytes

2001 ◽  
Vol 12 (7) ◽  
pp. 2075-2085 ◽  
Author(s):  
Marjan Huizing ◽  
Rangaprasad Sarangarajan ◽  
Erin Strovel ◽  
Yang Zhao ◽  
William A. Gahl ◽  
...  
Keyword(s):  
Dense Body ◽  
Multivesicular Bodies ◽  
Normal Pattern ◽  
Late Endosomes ◽  
Human Melanocytes ◽  
Hermansky Pudlak Syndrome ◽  
Functional Deficiency ◽  
Tyrosinase Related Protein

Patients with Hermansky-Pudlak syndrome type 2 (HPS-2) have mutations in the β3A subunit of adaptor complex-3 (AP-3) and functional deficiency of this complex. AP-3 serves as a coat protein in the formation of new vesicles, including, apparently, the platelet's dense body and the melanocyte's melanosome. We used HPS-2 melanocytes in culture to determine the role of AP-3 in the trafficking of the melanogenic proteins tyrosinase and tyrosinase-related protein-1 (TRP-1). TRP-1 displayed a typical melanosomal pattern in both normal and HPS-2 melanocytes. In contrast, tyrosinase exhibited a melanosomal (i.e., perinuclear and dendritic) pattern in normal cells but only a perinuclear pattern in the HPS-2 melanocytes. In addition, tyrosinase exhibited a normal pattern of expression in HPS-2 melanocytes transfected with a cDNA encoding the β3A subunit of the AP-3 complex. This suggests a role for AP-3 in the normal trafficking of tyrosinase to premelanosomes, consistent with the presence of a dileucine recognition signal in the C-terminal portion of the tyrosinase molecule. In the AP-3–deficient cells, tyrosinase was also present in structures resembling late endosomes or multivesicular bodies; these vesicles contained exvaginations devoid of tyrosinase. This suggests that, under normal circumstances, AP-3 may act on multivesicular bodies to form tyrosinase-containing vesicles destined to fuse with premelanosomes. Finally, our studies demonstrate that tyrosinase and TRP-1 use different mechanisms to reach their premelanosomal destination.

Sign in / Sign up

Export Citation Format

Share Document