1 Division of Nephrology, Department of Medicine, Vanderbilt University Veterans Affairs Medical Center, Nashville, Tennessee 37212; and Departments of 3 Pharmacology, Faculty of Medicine, and 2 Physiological Chemistry and Faculty of Pharmaceutical Sciences, Kyoto University, Kyoto, Japan 606
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ABSTRACT |
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PGF2 is one of the major
prostanoids produced by the kidney. The cellular effects of
PGF2
are mediated by a G protein-coupled transmembrane
receptor designated the FP receptor. Both in situ hybridization and
-galactosidase knocked into the endogenous FP locus were used to
determine the cellular distribution of the mouse FP receptor. Specific
labeling was detected in the kidney, ovary, and uterus. Abundant FP
expression in ovarian follicles and uterus is consistent with previous
reports of failed parturition in FP
/
mice. In the kidney,
coexpression of the mFP mRNA with the thiazide-sensitive cotransporter
defined its expression in the distal convoluted tubule (DCT). FP
receptor was also present in aquaporin-2-positive cortical collecting
ducts (CCD). No FP mRNA was detected in glomeruli, proximal tubules, or
thick ascending limbs. Intrarenal expression of the FP receptor in the
DCT and CCD suggests an important role for the FP receptor regulating water and solute transport in these segments of the nephron.
dinoprost; nephron; natriuresis; water
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INTRODUCTION |
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PROSTANOIDS,
including PGE2, PGD2, prostacyclin
(PGI2), TxA2, and PGF2, modulate
a diverse spectrum of physiological processes, including reproduction,
inflammation, microvascular resistance, and epithelial ion transport
rates (7, 33). Despite originating from a common
precursor, PGH2, the effects of these derivative
prostanoids may either oppose each other, as in the case of the
prothrombotic action of TxA2 vs. the antithrombotic effects
of PGI2 (16), or exert functionally
complementary effects such as the smooth muscle constrictor effects of
TxA2 and PGF2
(48). These
cellular and physiological effects are mediated by the selective
interaction of each prostanoid with unique G protein-coupled receptors
(GPCRs) (8, 33, 46). Genetic disruption of GPCR prostanoid
receptors has not only firmly established roles for these receptors as
critical mediators of prostanoid action, but it also revealed
significant new biology related to the roles of prostaglandins
(33, 46). In the case of the FP receptor for
PGF2
, these studies revealed that the FP receptor is
highly expressed in the ovary and its function is essential for normal
parturition (47).
The FP receptor is also highly expressed in the kidney (2,
44). Furthermore, PGF2 is a major product of
cyclooxygenase-mediated arachidonate metabolism in the kidney
(14), and renal synthesis of PGF2
is
regulated by sodium depletion, potassium depletion, and adrenal
steroids (35, 40). Infusion of exogenous
PGF2
modulates renal salt excretion and urine flow
(42). Despite this evidence supporting a role for the FP
receptor in the kidney, the intrarenal sites of expression or mechanism
of these PGF2
-activated GPCRs in the kidney remain
poorly characterized. The purpose of the present studies was to map the
intrarenal distribution of the FP receptor in the kidney.
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METHODS |
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Generation of RNA fragments.
RNA probes were generated by RT-PCR to amplify a 399-bp fragment
spanning the 5'-UTR to Arg100 in the coding region of the
mouse FP receptor cDNA from kidney RNA. The sense primer was
5'-AACCACTCAGTGGCTCAGGA-3', and the antisense primer was
5'-GCGGATCCAGTCTTTATC3'. The identity of the amplified product was
directly confirmed by sequencing and alignment with the mouse FP
receptor (BLAST, NCBI) and ligated into the transcription vector pCR2.1
(Invitrogen). The two distinct clones were isolated, which allowed
transcription of either the sense or antisense cDNAs using the T7
promoter. The plasmids were linearized and RNAs transcribed from the
flanking T7 promoter in the presence of [-35S]UTP. RNA
(5 × 105 cpm/µl) was used for in situ hybridization.
Tissue preparation. C57BL/6J mice weighing between 20 and 30 g were anesthetized using intraperitoneal ketamine and xylazine (200 mg and 15 mg/kg, respectively). After surgical anesthesia was achieved, mice were killed by cervical dislocation and kidney, stomach, liver, ovary, and uterus were harvested.
For in situ hybridization studies, tissues were fixed in 4% paraformaldehyde. Tissues were imbedded in paraffin and 7-µm sections were cut. Before hybridization, sections were deparaffinized, refixed in paraformaldehyde, treated with proteinase K (20 µg/ml), washed with PBS, refixed in 4% paraformaldehyde, and treated with triethanolamine plus acetic anhydride (0.25% vol/vol). Finally, sections were dehydrated in 100% ethanol. Anti-sense RNA was hybridized to the sections at 50-55°C for ~18 h as described previously (11). After hybridization, sections were washed at 50°C in 5× SSC + 10 mMPreparation of tissue for -galactosidase staining and
immunohistochemistry.
Multiple organs including liver, spleen, stomach, duodenum, lung, and
kidneys of the double transgenic mice were harvested at death. After
fixation with 4% paraformaldehyde plus 0.25% glutaraldehyde in PBS
for 2 h at 4°C, tissue sections were cut with a vibratome into
200-µm slices. To detect
-galactosidase (
-gal) activity, these
slices were bathed in permeabilization solution (2 mM
MgCl2, 0.01% sodium deoxycholate, 0.02% NP-40 in PBS) for
30 min × 2 and then stained with 1 mg/ml
5-bromo-4-chloro-3-indolyl-D-galactopyranoside (X-gal;
Sigma, St. Louis, MO) in staining solution (2 mM MgCl2, 5 mM potassium ferricyanide, potassium ferrocyanide, 20 mM Tris, pH 7.4 in PBS) at room temperature in the dark for 48 h (5, 36). Tissues were washed, dehydrated through graded ethanol series, and embedded in paraffin, using standard procedures. Serial 5-µm sections were cut and examined by light microscopy.
Immunostaining.
To define the nephron segments that expressed FP receptor mRNA, in situ
hybridization was followed by immunostaining of the tissue sections
with a rabbit anti-collecting duct antibody or a goat anti-human
Tamm-Horsfall antibody, which specifically recognizes medullary and
cortical thick ascending limb (mTAL and cTAL) as well as the early
portion of the distal tubule. To define the -gal-positive nephron
segments, sections were co-stained using a goat anti-human
Tamm-Horsfall antibody (1:2,500, Organon-Technika) that specifically
recognizes mTAL and cTAL as well as the early portion of the distal
tubule (28, 49). A commercially available anti-aquaproin-2 (AQP2) antibody was used to specifically identify collecting duct principal cells (AQP21-A, Anti-Rat AQP2 IgG no. 2, Alpha Diagnostic International, San Antonio, TX) (26). To define distal convoluted tubule segments (DCT), an
anti-thiazide-sensitive NaCl cotransporter (TSC) antibody was used
[generously provided by Dr. M. Knepper (30)]. Staining
was localized using a biotinylated anti-IgG secondary antibody applied
to
-gal-stained sections. Biotin was identified using streptavidin
coupled to horseradish peroxidase and was visualized with
diaminiobenzidine (Vector Vectastain ABC kit). Sections were viewed and
imaged with a Zeiss Axioskop and Spot-Cam digital camera (diagnostic instruments).
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RESULTS |
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Intrarenal distribution of the FP receptor.
Autoradiograms of the kidney, with an anti-sense FP receptor riboprobe
(Fig. 1), showed intense labeling of
subpopulations of epithelial tubules in the renal cortex. No
specific labeling was obtained with a sense mRNA probe (data not
shown). There was light and diffuse labeling of the outer medulla.
There was no detectable labeling of the papilla. A similar pattern of
FP mRNA expression was obtained by mapping -gal activity in
heterozygous FP +/
mice (Fig. 1B).
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Extrarenal tissues.
Abundant -gal expression was detected in stromal surrounding the
ureteral smooth muscle (Fig. 3).
Epididymus possesses endogenous
-gal activity in control animals,
complicating the interpretation of this tissues. However, this
endogenous activity was not present in any other organs from wild-type
animals examined including the distal vas deferens and luminal cells of
the testis where low levels of
-gal activity were detected. In the
female genital tract,
-gal expression was detected in ovary corpora
luteal cells and the smooth muscle cells lining the fallopian tubule
and uterus. Patches of intense
-gal labeling in tissues obtained
from FP +/
mice were associated with dermal hair follicles.
Liver failed to show any
-gal staining in hepatocytes, however,
labeling of vascular tissue was detected.
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DISCUSSION |
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The kidney is a site of robust prostaglandin synthesis and
expresses abundant prostanoid receptors (8, 10, 46). Renal expression of the FP, EP1, EP3, and TP receptor
mRNAs is particularly high (13, 25, 46). Furthermore, many
of the signaling pathways activated by this subset of receptors are
similar (12, 33), allowing for the possibility that these
receptors subserve functionally redundant roles. In this regard, it is
of note that striking similarities between the renal effects of
PGE2 and PGF2 exist. Similar to
PGE2, intrarenal infusion of PGF2
is
associated with natriuresis and diuresis, without altering glomerular
filtration rate or renal hemodynamics (50). Furthermore,
basolateral addition of either PGF2
or PGE2
can antagonize ADH-stimulated water absorption in microperfused
collecting ducts (43). Nonetheless, because PGF2
potently activates both prostaglandin FP and
EP3 receptors (1, 31), it is difficult to
attribute these renal affects specifically to activation of the FP
receptor. Furthermore, we are unaware of any published studies
examining the renal effects of FP receptor-selective agonists. For
these reasons, it is important that the present studies now demonstrate
segmental expression of FP receptor mRNA along the mouse nephron.
The present studies used both in situ hybridization and a -gal
reporter knocked into the endogenous FP locus (47) to map the distribution of the FP receptor. FP receptor expression determined using these two different techniques was mutually supportive. In the
kidney, the most intense labeling was detected over a subpopulation of
cells in the cortex. The mouse FP receptor mRNA was most abundant in
distal nephron segments colabeling with antibodies to the TSC1 and the
vasopressin-stimulated water channel AQP2. In mice, TSC1 is expressed
only in the DCT, where it mediates NaCl absorption (15).
FP receptor activation could inhibit salt absorption in this nephron
segment, thereby contributing to the natriuretic effects of
PGF2
. The DCT is also a major site of calcium absorption
(32, 38), so it is also conceivable that
PGF2
plays a role in modulating Ca2+
absorption by the kidney. Similarly, the detection of the FP receptor
in AQP2-immunoreactive cells demonstrates its expression in the
collecting duct (20, 21), representing another site where
its activation could contribute to PGF2
-induced
natriuresis and diuresis.
Although the presence of low levels of FP mRNA in the thick ascending
limb cannot be excluded, it seems clear that the expression of FP
transcripts in the thick ascending limb is markedly less than in either
the DCT or cortical collecting duct (CCD). Interestingly, there appears
to be a gradient for the intensity of FP gene expression along the
distal tubule, with greater levels of expression in the DCT/connecting
tubule, > CCD >>MCD. This is in contrast to EP3 mRNA,
which is more abundant in medullary CD than CCD and expressed in mTAL
as well (9, 11, 45). Finally, the EP1 receptor
is most abundant in the papillary collecting duct (25, 45). This axial heterogeneity of the prostanoid receptors is consistent with a major role for PGF2 action in the
renal cortex as opposed to the medulla, where PGE2 action
may predominate.
The cellular effects of the FP receptor in distal renal epithelia
remain uncharacterized. In fibroblasts, smooth muscle cells, or cells
transfected with the FP receptor, PGF2 activates a
signaling pathway coupled to increased cell calcium and
phosphatidylinositol hydrolysis (3, 23, 24). A similar
signaling pathway is activated by the EP1 receptor in the
collecting duct, and this signaling pathway contributes the capacity of
PGE2 to inhibit vasopressin-stimulated water flow and
sodium absorption (19, 25, 27). Activation of a
Ca2+-coupled signaling pathway by the FP receptor in the
collecting duct could therefore contribute to natriuresis and diuresis
caused by PGF2
infusion. Other studies in transfected
cells show that the FP receptor can activate a
-catenin-coupled
signaling pathway (18), however, the significance of this
pathway in differentiated renal epithelial is uncharacterized.
Alternatively, of the known prostanoid receptors, the FP receptor
protein sequence is most closely related to the EP3 receptor
(37) that preferentially couples to Gi and inhibits
vasopressin-stimulated cAMP generation and water flow via this
pertussis toxin-sensitive mechanism (25, 27, 41).
Additional studies will be required to determine which, if any of these
pathways, is activated by the FP receptor in these nephron segments.
As previously reported, -gal expression was abundant in ovarian
corpus luteum where FP activation appears to play a critical role in
parturition, initiating the perinatal decline in progesterone secretion
(47). The expression of
-gal in corpora luteal cells provides additional validation for concordance of
-gal expression with FP mRNA expression since abundant expression FP mRNA has been
demonstrated in corpora lutea of mice by both techniques (44,
47). FP receptor is also expressed in uterine smooth muscle (6), consistent with the present studies
demonstrating
-gal in this tissue. Robust
-gal activity was also
detected along the male genital tract, particularly in the epithelia
lining the lumen of the epididymis and vas deferens. Because the
epididymis possesses endogenous
-gal activity (17, 22)
detected in the wild type (not shown), the significance of staining in
this segment of the male genital tract remains uncertain. In contrast,
we did not detect
-gal activity in wild-type testis, so FP recetor
could be expressed in this tissue and its activation contributes to previous reports that in vivo administration of PGF2
to
mice causes atrophy of epididymal epithelium (39).
-Gal expression was not apparent in hepatocytes, despite reported
effects of PGF2
on hepatic glucose output
(34), consistent with the possibility of an unrelated
receptor or pharmacological target for PGF2
in mediating
these effects. Interestingly, intense expression of
-gal activity
was observed in hepatic vasculature, where it could mediate the
capacity of PGF2
to induce nitric oxide-dependent
vasodilatation (4). Finally, the present studies also
identified a restricted pattern of FP receptor in skin, particularly in
the dermal papillae. This site of expression may be important in
mediating the stimulatory effect of latanaprost, an FP-selective agonist, on hair growth (29).
In summary, the present studies demonstrate high levels of expression
of mRNA for the FP receptor in kidney distal tubules, including the DCT
and CCD. The intrarenal distribution of FP receptor mRNA corresponds
with the known effects of PGF2 on salt and water
transport in the kidney. The FP receptor is expressed along both male
and female genitourinary tracts.
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ACKNOWLEDGEMENTS |
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This work was funded in part by an American Heart Association fellowship award (to O. Saito), an American Diabetes Association award (to Y. F. Guan), and VA Merit Award and National Institutes of Health Grant DK-37097 (to M. D. Breyer).
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FOOTNOTES |
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Present address of M. Kömhoff: Dept. of Pediatrics, Philips-Univ. Marburg, Deutschhausstrasse 12, D35053 Marburg, Germany.
Address for reprint requests and other correspondence: M. D. Breyer, Division of Nephrology and Dept. of Medicine, Vanderbilt Univ., F427-ACRE Bldg., Dept. of Veterans Affairs Medical Center, Nashville, TN 37212 (E-mail: Matthew.Breyer{at}vanderbilt.edu).
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
First published March 11, 2003;10.1152/ajprenal.00441.2002
Received 30 December 2002; accepted in final form 9 February 2003.
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