Subtype-selective expression of the five somatostatin receptors (hSSTR1- 5) in human pancreatic islet cells: A quantitative double-label immunohistochemical analysis

Ujendra Kumar, Ramakrishnan Sasi, Sundar Suresh, Amit Patel, Muthusamy Thangaraju, Peter Metrakos, Shutish C. Patel, Yogesh C. Patel

Research output: Contribution to journalArticle

208 Citations (Scopus)

Abstract

We have developed a panel of rabbit polyclonal antipeptide antibodies against the five human somatostatin receptor subtypes (hSSTR1-5) and used them to analyze the pattern of expression of hSSTR1-5 in normal human islet cells by quantitative double-label confocal fluorescence immunocytochemistry. All five hSSTR subtypes were variably expressed in islets. The number of SSTR immunopositive cells showed a rank order of SSTR1 > SSTR5 > SSTR2 > SSTR3 > SSTR4. SSTR1 was strongly colocalized with insulin in all β-cells. SSTR5 was also an abundant isotype, being colocalized in 87% of β-cells. SSTR2 was found in 46% of β-cells, whereas SSTR3 and SSTR4 were relatively poorly expressed. SSTR2 was strongly colocalized with glucagon in 89% of α-cells, whereas SSTR5 and SSTR1 colocalized with glucagon in 35 and 26% of α-cells, respectively. SSTR3 was detected in occasional α-cells, and SSTR4 was absent. SSTR5 was preferentially expressed in 75% of SST-positive cells and was the principal δ-cell SSTR subtype, whereas SSTR1-3 were colocalized in only a few δ-cells, and SSTR4 was absent. These studies reveal predominant expression of SSTR1, SSTR2, and SSTR5 in human islets. β-Cells, α-cells, and δ-cells each express multiple SSTR isoforms, β-cells being rich in SSTR1 and SSTR5, α-cells in SSTR2, and δ-cells in SSTR5. Although there is no absolute specificity of any SSTR for an islet cell type, SSTR1 is β-cell selective, and SSTR2 is α-cell selective. SSTR5 is well expressed in β- cells and δ-cells and moderately well expressed in α-cells, and thereby it lacks the islet cell selectivity displayed by SSTR1 and SSTR2. Subtype- selective SSTR expression in islet cells could be the basis for preferential insulin suppression by SSTR1-specific ligands and of glucagon inhibition by SSTR2-selective compounds.

Original languageEnglish (US)
Pages (from-to)77-85
Number of pages9
JournalDiabetes
Volume48
Issue number1
DOIs
StatePublished - Jan 1 1999
Externally publishedYes

Fingerprint

Islets of Langerhans
somatostatin receptor 5
Glucagon
Insulin
somatostatin receptor type 1
Somatostatin Receptors

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism

Cite this

Subtype-selective expression of the five somatostatin receptors (hSSTR1- 5) in human pancreatic islet cells : A quantitative double-label immunohistochemical analysis. / Kumar, Ujendra; Sasi, Ramakrishnan; Suresh, Sundar; Patel, Amit; Thangaraju, Muthusamy; Metrakos, Peter; Patel, Shutish C.; Patel, Yogesh C.

In: Diabetes, Vol. 48, No. 1, 01.01.1999, p. 77-85.

Research output: Contribution to journalArticle

Kumar, Ujendra ; Sasi, Ramakrishnan ; Suresh, Sundar ; Patel, Amit ; Thangaraju, Muthusamy ; Metrakos, Peter ; Patel, Shutish C. ; Patel, Yogesh C. / Subtype-selective expression of the five somatostatin receptors (hSSTR1- 5) in human pancreatic islet cells : A quantitative double-label immunohistochemical analysis. In: Diabetes. 1999 ; Vol. 48, No. 1. pp. 77-85.
@article{8af55c346e1f4b39b9250a823152ae03,
title = "Subtype-selective expression of the five somatostatin receptors (hSSTR1- 5) in human pancreatic islet cells: A quantitative double-label immunohistochemical analysis",
abstract = "We have developed a panel of rabbit polyclonal antipeptide antibodies against the five human somatostatin receptor subtypes (hSSTR1-5) and used them to analyze the pattern of expression of hSSTR1-5 in normal human islet cells by quantitative double-label confocal fluorescence immunocytochemistry. All five hSSTR subtypes were variably expressed in islets. The number of SSTR immunopositive cells showed a rank order of SSTR1 > SSTR5 > SSTR2 > SSTR3 > SSTR4. SSTR1 was strongly colocalized with insulin in all β-cells. SSTR5 was also an abundant isotype, being colocalized in 87{\%} of β-cells. SSTR2 was found in 46{\%} of β-cells, whereas SSTR3 and SSTR4 were relatively poorly expressed. SSTR2 was strongly colocalized with glucagon in 89{\%} of α-cells, whereas SSTR5 and SSTR1 colocalized with glucagon in 35 and 26{\%} of α-cells, respectively. SSTR3 was detected in occasional α-cells, and SSTR4 was absent. SSTR5 was preferentially expressed in 75{\%} of SST-positive cells and was the principal δ-cell SSTR subtype, whereas SSTR1-3 were colocalized in only a few δ-cells, and SSTR4 was absent. These studies reveal predominant expression of SSTR1, SSTR2, and SSTR5 in human islets. β-Cells, α-cells, and δ-cells each express multiple SSTR isoforms, β-cells being rich in SSTR1 and SSTR5, α-cells in SSTR2, and δ-cells in SSTR5. Although there is no absolute specificity of any SSTR for an islet cell type, SSTR1 is β-cell selective, and SSTR2 is α-cell selective. SSTR5 is well expressed in β- cells and δ-cells and moderately well expressed in α-cells, and thereby it lacks the islet cell selectivity displayed by SSTR1 and SSTR2. Subtype- selective SSTR expression in islet cells could be the basis for preferential insulin suppression by SSTR1-specific ligands and of glucagon inhibition by SSTR2-selective compounds.",
author = "Ujendra Kumar and Ramakrishnan Sasi and Sundar Suresh and Amit Patel and Muthusamy Thangaraju and Peter Metrakos and Patel, {Shutish C.} and Patel, {Yogesh C.}",
year = "1999",
month = "1",
day = "1",
doi = "10.2337/diabetes.48.1.77",
language = "English (US)",
volume = "48",
pages = "77--85",
journal = "Diabetes",
issn = "0012-1797",
publisher = "American Diabetes Association Inc.",
number = "1",

}

TY - JOUR

T1 - Subtype-selective expression of the five somatostatin receptors (hSSTR1- 5) in human pancreatic islet cells

T2 - A quantitative double-label immunohistochemical analysis

AU - Kumar, Ujendra

AU - Sasi, Ramakrishnan

AU - Suresh, Sundar

AU - Patel, Amit

AU - Thangaraju, Muthusamy

AU - Metrakos, Peter

AU - Patel, Shutish C.

AU - Patel, Yogesh C.

PY - 1999/1/1

Y1 - 1999/1/1

N2 - We have developed a panel of rabbit polyclonal antipeptide antibodies against the five human somatostatin receptor subtypes (hSSTR1-5) and used them to analyze the pattern of expression of hSSTR1-5 in normal human islet cells by quantitative double-label confocal fluorescence immunocytochemistry. All five hSSTR subtypes were variably expressed in islets. The number of SSTR immunopositive cells showed a rank order of SSTR1 > SSTR5 > SSTR2 > SSTR3 > SSTR4. SSTR1 was strongly colocalized with insulin in all β-cells. SSTR5 was also an abundant isotype, being colocalized in 87% of β-cells. SSTR2 was found in 46% of β-cells, whereas SSTR3 and SSTR4 were relatively poorly expressed. SSTR2 was strongly colocalized with glucagon in 89% of α-cells, whereas SSTR5 and SSTR1 colocalized with glucagon in 35 and 26% of α-cells, respectively. SSTR3 was detected in occasional α-cells, and SSTR4 was absent. SSTR5 was preferentially expressed in 75% of SST-positive cells and was the principal δ-cell SSTR subtype, whereas SSTR1-3 were colocalized in only a few δ-cells, and SSTR4 was absent. These studies reveal predominant expression of SSTR1, SSTR2, and SSTR5 in human islets. β-Cells, α-cells, and δ-cells each express multiple SSTR isoforms, β-cells being rich in SSTR1 and SSTR5, α-cells in SSTR2, and δ-cells in SSTR5. Although there is no absolute specificity of any SSTR for an islet cell type, SSTR1 is β-cell selective, and SSTR2 is α-cell selective. SSTR5 is well expressed in β- cells and δ-cells and moderately well expressed in α-cells, and thereby it lacks the islet cell selectivity displayed by SSTR1 and SSTR2. Subtype- selective SSTR expression in islet cells could be the basis for preferential insulin suppression by SSTR1-specific ligands and of glucagon inhibition by SSTR2-selective compounds.

AB - We have developed a panel of rabbit polyclonal antipeptide antibodies against the five human somatostatin receptor subtypes (hSSTR1-5) and used them to analyze the pattern of expression of hSSTR1-5 in normal human islet cells by quantitative double-label confocal fluorescence immunocytochemistry. All five hSSTR subtypes were variably expressed in islets. The number of SSTR immunopositive cells showed a rank order of SSTR1 > SSTR5 > SSTR2 > SSTR3 > SSTR4. SSTR1 was strongly colocalized with insulin in all β-cells. SSTR5 was also an abundant isotype, being colocalized in 87% of β-cells. SSTR2 was found in 46% of β-cells, whereas SSTR3 and SSTR4 were relatively poorly expressed. SSTR2 was strongly colocalized with glucagon in 89% of α-cells, whereas SSTR5 and SSTR1 colocalized with glucagon in 35 and 26% of α-cells, respectively. SSTR3 was detected in occasional α-cells, and SSTR4 was absent. SSTR5 was preferentially expressed in 75% of SST-positive cells and was the principal δ-cell SSTR subtype, whereas SSTR1-3 were colocalized in only a few δ-cells, and SSTR4 was absent. These studies reveal predominant expression of SSTR1, SSTR2, and SSTR5 in human islets. β-Cells, α-cells, and δ-cells each express multiple SSTR isoforms, β-cells being rich in SSTR1 and SSTR5, α-cells in SSTR2, and δ-cells in SSTR5. Although there is no absolute specificity of any SSTR for an islet cell type, SSTR1 is β-cell selective, and SSTR2 is α-cell selective. SSTR5 is well expressed in β- cells and δ-cells and moderately well expressed in α-cells, and thereby it lacks the islet cell selectivity displayed by SSTR1 and SSTR2. Subtype- selective SSTR expression in islet cells could be the basis for preferential insulin suppression by SSTR1-specific ligands and of glucagon inhibition by SSTR2-selective compounds.

UR - http://www.scopus.com/inward/record.url?scp=0032908805&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0032908805&partnerID=8YFLogxK

U2 - 10.2337/diabetes.48.1.77

DO - 10.2337/diabetes.48.1.77

M3 - Article

C2 - 9892225

AN - SCOPUS:0032908805

VL - 48

SP - 77

EP - 85

JO - Diabetes

JF - Diabetes

SN - 0012-1797

IS - 1

ER -