β-adrenergic induction of a cysteine-proteinase-inhibitor mRNA in rat salivary glands

Transcripts encoding the cysteine-proteinase inhibitor rat cystatin S are induced in submandibular and parotid glands by the beta-adrenergic agonist isoproterenol (isoprenaline). High levels of cystatin S mRNA persist in glands of chronically treated animals for 6 days after discontinuation of the catecholamine, indicating a long half-life of the mRNA. Post-transcriptionally the size of the mRNA decreases, owing to a shortening of the poly(A) tail.

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Cloning and sequencing of cDNA encoding a rat salivary cysteine proteinase inhibitor inducible by beta-adrenergic agonists.

Journal of Biological Chemistry ◽

10.1016/s0021-9258(19)81334-0 ◽

1988 ◽

Vol 263 (34) ◽

pp. 18133-18137 ◽

Cited By ~ 2

Author(s):

P A Shaw ◽

J L Cox ◽

T Barka ◽

Y Naito

Keyword(s):

Proteinase Inhibitor ◽

Cysteine Proteinase ◽

Cysteine Proteinase Inhibitor ◽

Adrenergic Agonists ◽

Cloning And Sequencing ◽

Beta Adrenergic ◽

Beta Adrenergic Agonists

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Induction of Type 2 Salivary Cystatin in Immunological and Chemical Kidney Injury

Critical Reviews in Oral Biology & Medicine ◽

10.1177/10454411930040034201 ◽

1993 ◽

Vol 4 (3) ◽

pp. 553-563 ◽

Cited By ~ 4

Author(s):

R.E. Cohen ◽

G.S. Bedi ◽

M.E. Neiders ◽

B. Noble

Keyword(s):

Salivary Glands ◽

Proteinase Inhibitor ◽

Tissue Injury ◽

Potassium Dichromate ◽

Cysteine Proteinase ◽

Cysteine Proteinase Inhibitor ◽

Kidney Tubule ◽

Local Response ◽

Specific Staining

We have previously reported that isoproterenol induces type 2 salivary cystatin in both submandibular glands and kidney tubule cells of rats but not in any other organs examined. In the present study, we investigated whether this salivary protein is induced in other conditions that show kidney tubule injury. Immunocytochemistry, using a monospecific antiserum to this cystatin, revealed specific staining within the proximal tubule epithelium of the cortex as well as in the inner and outer stripe of the medulla of immunologically and chemically injured rats. Cystatin could not be detected in kidneys from healthy rats by means of immunocytochemistry. Weak staining was found in 3/3 kidneys of rats treated with turpentine and in 5/5 animals treated with potassium dichromate. In rats treated with puromycin, cystatin could not be demonstrated in 5/5 animals having proteinuria of less than 100 mg/24 h; however, moderate staining was observed in 4/5 puromycin-treated rats having proteinuria greater than 100 mg/24 h. In Heymann nephritis, cystatin was present in 7/31 kidneys with proteinuria lasting 6 to 15 weeks and in none (0/ 7) with proteinuria of shorter duration. Strong staining was also observed in 10/10 kidneys from rats with moderate-to-severe chronic serum sickness. This study shows that elaboration of type 2 cystatin in rats is not limited to salivary glands and, with our previous study, suggests that induction of this cysteine proteinase inhibitor may represent a local response to generalized tissue injury in both submandibular and renal tissues. These findings further demonstrate that induction of cystatin in salivary glands is not unique to these glands and suggest that induction of this cysteine proteinase inhibitor may represent a local response to tissue injury caused by diverse mechanisms.

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Expression and induction by β-adrenergic agonists of the cystatin S gene in submandibular glands of developing rats

Biochemical Journal ◽

10.1042/bj2650115 ◽

1990 ◽

Vol 265 (1) ◽

pp. 115-120 ◽

Cited By ~ 26

Author(s):

P A Shaw ◽

T Barka ◽

A Woodin ◽

B S Schacter ◽

J L Cox

Keyword(s):

Cysteine Proteinase ◽

Cysteine Proteinase Inhibitor ◽

Parotid Glands ◽

High Concentration ◽

Adult Rats ◽

Beta Adrenergic ◽

Submandibular Glands ◽

S Gene ◽

Old Rats

Repeated administration of the beta-adrenergic agonist isoprenaline (isoproterenol, IPR), which produces hypertrophic/hyperplastic enlargements of rat submandibular and parotid glands, induces synthesis of a secretory protein shown to be a cysteine proteinase inhibitor, rat cystatin S. In the current study, Northern blot and hybridizations in situ were carried out to establish the developmental and beta-adrenergic regulation of the expression of the cystatin S gene. Cystatin S mRNA was not detected in submandibular glands of 20-day-old fetuses, nor in the glands of newborn or 10-day-old rats. However, steady-state levels of cystatin S mRNA increased between 21 and 28 days, reaching a conspicuously high concentration at 28 days; cystatin S mRNA then declined rapidly to a barely detectable level in glands of 32-day-old rats. IPR administration for 4 days induced high levels of cystatin S mRNA in submandibular glands of developing and adult rats. In both prepubertal and mature animals, induction of cystatin S mRNA in submandibular glands was more pronounced in female than in male animals. Hybridizations in situ revealed cystatin S mRNA only in acinar but not in duct cells of the submandibular gland. Developmentally, expression of the cystatin S gene coincided with acinar cell differentiation. These data suggest a complex neural, hormonal and developmental regulation of salivary cystatin genes.

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